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3154 MSK > Pharmaco: NSAIDs > Flashcards

Pharmaco: NSAIDs Flashcards

1
Q

Do a quick comparison of NSAIDs, Paracetamol, and Opioids

A

NSAIDs: block acute inflammatory response at the site of injury

Paracetamol: modulates how the brain interprets pain signals

Opioids: blocks transmission and signaling of pain through the nerve at the spinothalamic relay and the CNS

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2
Q

Recap: 4 components of acute inflammatory response

A
  • Warmth
  • Redness
  • Swelling
  • Pain
  • Loss of function (additional component)
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3
Q

Describe the pathways of phospholipase A2 (from cell membrane phospholipids)

A

Phospholipase A2 => Arachidonic acid (AA)

AA has three pathways

  1. 15-Lipoxygenase => Lipoxins
  2. Cyclooxygenase (COX) => Prostanoids
  • more selective for acute inflammatory response
  1. 5-Lipoxygenase => Leukotrienes
  • more involved in chronic inflammatory + immune responses

Lipoxins, Prostanoids, and Leukotrienes are known as Eisosanoids, involved in the inflammation process

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4
Q

Difference between steroids and NSAIDs MOA

A

Steroids block Phospholipase A2, thereby blocking all the subsequent pathways (potent anti-inflammatory response, potentially immunosuppressive when used long-term)

NSAIDs block cyclooxygenase (COX) and therefore the prostaglandins production (selective for acute inflammation)

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5
Q

What are the prostaglandins produced by COX?

A

PGI2 (prostacyclin)

  • inhibit platelet aggregation (antiplatelet)
  • vasodilation
  • might expect more in closed wounds, infections etc.

PGE2 (classical prostaglandins)

  • directly involved in acute inflammation
  • increased vascular permeability (swelling, edema)
  • pain
  • vasodilation (warmth, redness, swelling)

TXA2 (thomboxanes)

  • platelet aggregation
  • vasoconstriction
  • might expect more in open wounds
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6
Q

Explain the analgesic effects of Aspirin (NSAID)

Why is NSAID only sufficient for mild-mod pain?

A

NSAIDs block the production of prostaglandins, which sensitize the nociceptive fibers to stimulation by other inflammatory mediators (e.g., bradykinin, leukotrienes)

Block of sensitization rather than direct nociceptive activation explains why NSAIDs have an ‘analgesic ceiling’ (i.e. there may still be too much bradykinin, leukotrienes) - still pain signaling by other inflammatory mediators

NSAIDs also have additional analgesic actions in the CNS

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7
Q

Explain the antipyretic effects of Aspirin (NSAID)

A

In infections/tissue damage/inflammation, there is incr in neutrophils, leading to incr release of cytokines which increases the expression of COX in the hypothalamus of the brain. This leads to increase PGE2 that results in warmth and fever

NSAIDs are antipyretic as they inhibit COX thereby reducing PGE2 production and alleviating the fever

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8
Q

Explain Aspirin as an antiplatelet

A

Aspirin is an irreversible COX inhibitor, inhibits COX-1 (TXA2) more than COX-2 (PGI2), therefore inhibiting platelet production of TXA2

*Recall pdn of TXA2 in platelets (1-2 weeks), pdn of PGI2 by endothelial cells (few hours)

*antiplatelet dose is low

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9
Q

Therefore, NSAIDs (such as aspirin) are:

A
  • anti-inflammatory (block PGE2, PGI2, TXA2)
  • analgesic (block sensitization)
  • antipyretic (block PGE2)
  • antiplatelet (aspirin is an irreversible COX inhibitor, block TXA2 > PGI2)
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10
Q

Adverse effects of Aspirin are ________

A

dose-dependent

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11
Q

What are some side effects at low doses (therapeutic range for NSAID)?

A

SEs are due to COX inhibition (up to 1g)

  • Gastric intolerance
  • Bleeding
  • Hypersensitivity
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12
Q

What are some side effects at high doses?

A

SEs are due to salicylate toxicity

To progressively higher doses (1g and onwards):

  • Tinnitus
  • Uricosuric
  • Central hyperventilation
  • Respiratory alkalosis
  • Fever, dehydration
  • Metabolic acidosis
  • Respiratory acidosis
  • Hypoprothrombinemia
  • Vasomotor collapse
  • Coma
  • Renal failure
  • Respiratory failure
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13
Q

What is Reye’s syndrome?

What are the symptoms?

Who is at increased risk of it?

A

Rare, but life-threatening condition

Swelling of the brain (encephalitis) and liver

Symptoms include:

  • Severe vomiting with viral symptoms such as fever, aches, pain
  • Personality/behavior changes
  • Listlessness
  • Delirium
  • Convulsions
  • Loss of consciousness

Increased risk:

  • Children with viral infections taking Aspirin

Therefore, aspirin is now contraindicated in children

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14
Q

Effectiveness of Naproxen

A
  • More effective in women (free fraction >40% higher)
  • Often use for dysmenorrhea
  • Half-life 12-14h (dosed two times daily)

note that most older NSAIDs have shorter half-life and are dosed more frequently; Naproxen is an exception (BD)

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15
Q

Effectiveness of Diclofenac

  • in terms of half-life
A
  • Short plasma half-life <2h, therefore low GI risk, low systemic SEs
  • Longer half-life in synovial fluid, hence useful in inflammatory joint diseases
  • Can be applied topically
  • Additional CVD risk if taken systemically
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16
Q

Effectiveness of Indomethacin

A
  • Strongly anti-inflammatory due to additional steroid-like phospholipase A2 inhibition (thus, it is useful in rheumatic joint conditions)
  • However, less frequently 1st choice due to reported CNS adverse effects: 15-25% report headache, altered mental status, confusion or depression, also have cases of psychosis and hallucinations
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17
Q

[Adverse effects of NSAIDs due to COX-inhibition]

  • Explain the mechanism of GI adverse effects
A

In normal circumstances,

  • Prostaglandins (PGE2) reduces gastric acid secretions, increases mucosal blood flow, increases mucus secretion, and increases bicarbonate secretion

When NSAID is administered,

  • PGE2 is inhibited
  • Common SEs: dyspepsia, nausea, vomiting, anorexia, abdominal pain
  • More serious: Risk of peptic ulcer formation, and hemorrhagic risk, GI bleed/ulcer/perforation
  • Risk of peptic ulcer greatly increased if used for >5days
  • Coupled with antiplatelet effects (if aspirin) => incr risk of bleeding

Therefore, older NSAIDs may not be appropriate for long-term use in chronic arthritis due to risk of GI ulcer and bleed

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18
Q

[Adverse effects of NSAIDs due to COX-inhibition]

  • Risk factors for GI toxicity - GI bleed, perforation, ulceration (IC16)
A
  • > 65y
  • History of ulcer
  • Use of high dose/chronic NSAID
  • Concurrent glucocorticoids/antiplatelets/anticoagulants

High risk:
- 3 or more of the 4 risk factors OR
- history of complicated ulcer (ulcer + bleed)

If high risk, choose coxib, consider adding PPI
Other considerations: Ibuprofen has less GI SEs than Naproxen; use paracetamol if possible

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19
Q

[Adverse effects of NSAIDs due to COX-inhibition]

  • When is urgent referral needed for suspected NSAID-induced GI complications? (IC16)
A
  • Fatigue symptoms
  • Severe dyspepsia
  • Signs of GI bleeding (melena - black tarry stools, coughing out coffee-ground-like substance)
  • Unexplained blood loss anemia
  • Iron deficiency
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20
Q

[Adverse effects of NSAIDs due to COX-inhibition]

  • Explain the mechanism of renal adverse effects
A

Inhibition of PGE2 and PGI2 alters the renal blood flow dynamics:

PGE2 actions

  • Inhibits sodium reabsorption in the thick ascending limb (25% of Na+ reabsorbed)

Inhibition of PGE2 production

  • Sodium retention
  • Water retention
  • Peripheral edema (esp seen in long acting NSAIDs such as Naproxen and Celecoxib)
  • Hypertension

PGI2 actions

  • PGI2 stimulates secretion of renin and hence aldosterone
  • Aldosterone increases Na+ reabsorption and K+ excretion

Inhibition of PGI2 production

  • Suppression of renin and aldosterone secretion (therefore prevents reabsorption of Na+ in the distal convoluted tubule, but only 1-2%)
  • Hyperkalemia (incr K+ retention)
  • Acute renal failure
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21
Q

How do PG and Ang II play a role in kidney function?

A

PG - vasodilation of afferent arteriole, increase GFR, increase RBF

Ang II - vasoconstriction of efferent arteriole, increase GFR, decrease RBF

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22
Q

What is the triple whammy?
What do the cause?
How do the cause it?

A

NSAID + Diuretics + ACE inhibitors

These drugs used in hypertension and heart failure reduce kidney function and increase risk of acute kidney injury

NSAIDs:

  • Inhibit prostaglandins, inhibits vasodilation of afferent arterioles
  • meaning causes vasoconstriction of afferent arteriole which decreases GFR and renal blood flow

Diuretics:

  • Volume depletion, reduce renal blood flow

ACEi:

  • Inhibits angiotensin-converting enzyme, decreases angiotensin II, inhibit vasoconstriction of efferent arterioles
  • Vasodilation of efferent decreases GFR, increases renal blood flow
23
Q

Risk factors for renal toxicity: NSAID-induced acute kidney injury

Also combined with IC16

A
  • Increasing age (>65), chronic hypertension and atherosclerosis
  • Pre-existing glomerular disease or renal insufficiency
  • Volume depletion (true - e.g., diuretic use, blood loss, diarrhea, sepsis VS effective arterial depletion - e.g., cirrhosis, heart failure, nephrotic syndrome)
  • Use of ACEi or ARB
  • Use of triple whammy

(IC16) additional risk factors:

  • CKD (may use if really needed for <5-7 days in GFR <60ml/min; avoid use in GFR <15ml/min)
  • Severe hypercalcemia/renal artery stenosis
  • Drug-induced nephrotoxicity: aminoglycosides, amphotericin B, radiocontrast material
  • Hyperkalemia
  • Hyponatremia
24
Q

Which risk factors for renal toxicity should avoid PO NSAID? (IC16)

A
  • Volume depletion (true - e.g., diuretic use, blood loss, diarrhea, sepsis VS effective - e.g., cirrhosis, heart failure)
  • Use of ACEi or ARB, also hyperkalemia & hyponatremia
  • Use of triple whammy
  • Severe hypercalcemia/renal artery stenosis
  • Drug-induced nephrotoxicity: aminoglycosides, amphotericin B, radiocontrast material

Use topical NSAID instead (but avoid in nephrotic syndrome or hx of NSAID-induced AIN)

If use is unavoidable, monitor SCr and electrolytes (this includes: SCr, BUN, hyperkalemia, incr BP, peripheral edema, weight gain)

Still may use PO:

  • CKD (depending on eGFR)
  • > 65y

NSAID should be discontinued if pt has AKI

25
Q

Explain how the following risk factor contributes to NSAID-induced AKI

  • Increasing age (>65), chronic hypertension and atherosclerosis
A

Narrowing of renal afferent arterioles, dcr GFR

26
Q

Explain how the following risk factor contributes to NSAID-induced AKI

  • Pre-existing glomerular disease or renal insufficiency
A

Reduce capacity for renal afferent dilation, dcr GFR

27
Q

Explain how the following risk factor contributes to NSAID-induced AKI

  • Volume depletion (true - e.g., diuretic use, blood loss VS effective - e.g., cirrhosis, heart failure)
A

Decrease renal blood flow, lowers afferent glomerular arteriolar pressure, stimulates secretion of angiotensin II (which vasoconstricts the efferent to increase GFR)

28
Q

Explain how the following risk factor contributes to NSAID-induced AKI

  • Use of ACEi or ARB
  • Use of triple whammy
A

NSAIDs:

  • Inhibit prostaglandins, inhibits vasodilation of afferent arterioles
  • meaning causes vasoconstriction of afferent arteriole which decreases glomerulus pressure, renal blood flow, and GFR

Diuretics:

  • Volume depletion, reduce renal blood flow

ACEi and ARBs

  • Inhibits angiotensin-converting enzyme, decreases angiotensin II, inhibit vasoconstriction of efferent arterioles
  • Vasodilation of efferent decreases GFR
29
Q

[Adverse effects of NSAIDs due to COX-inhibition]

Explain the mechanism of **NSAID-induced bronchospasm **in pt with hx of asthma as well as mechanism of pseudo-allergy

A

Mechanism:

COX inhibition causes shunting of arachidonic acid into the leukotriene pathway, causing excess leukotriene acts on LTD4, which can lead to bronchospasm in asthmatics and allergic reaction-like symptoms

Unsure MOA: also consider COX-1 inhibition causes less PGE2 production, leading to bronchospasm (since PGE2 is a bronchodilator)

Recall that leukotriene is involved in chronic inflammation + immune responses

CAUTION: in patients with the sensitivity triad of asthma, chronic urticaria, nasal polyps

Effects are much stronger for Aspirin as it is an irreversible COX-inhibitor, aka aspirin-sensitive asthma

30
Q

[Adverse effects of NSAIDs due to COX-inhibition]

Explain pseudo-allergic reaction vs true allergy

(combine with IC16)

A

Pseudo-allergy

  • Non-immunogenic
  • Symptoms: skin rashes, swelling, itching, nasal congestion, anaphylactic shock
  • Include reactions such as: aspirin-exacerbated respiratory disease AERD (wheezing, rhinitis, nasal congestion, SOB, asthma exacerbation)
  • Means that patient is sensitive to COX-inhibition and excess leukotriene
  • May have same reaction across different non-selective NSAIDs (avoid), coxibs can be used with caution

Allergy

  • Immunogenic, IgE mediated
  • Possible reactions include: urticaria, angioedema, anaphylaxis
  • Avoid ALL NSAIDs and coxibs if anaphylaxis involved (even though true allergy is only to the specific NSAID based on chemical structure)
31
Q

[Adverse effects of NSAIDs due to COX-inhibition]

Explain bleeding adverse effect of NSAIDs

Caution in which populations

IC16

A

(While GI bleed is mediated by inhibition of PGE2 production)

Bleeding events are due to:

  • failure of hemostasis, bruising due to COX1 > COX2 inhibition
  • COX1 inhibition blocks TXA2 which is involved in platelet aggregation, hence causing increased risk of bleeding
  • effect stronger for aspirin, an irreversible cox-inhibitor

Caution:

  • Surgical procedures when pt alr on NSAIDs (stop 3 days prior to surgery; aspirin stop 1 week prior)
  • Incr bleeding risk in combi with antiplatelet therapy (e.g., clopidogrel)
32
Q

Difference between COX-1 and COX-2

A

Constitutive COX-1

  • more involved in normal physiological functions
  • found in intestines, platelets, stomach, kidney
  • produces TXA2, PGI2, PGE2

Constitutive COX-2

  • involved in normal physiological functions
  • found in CNS, kidneys, female reproductive tract, synovium

Inducible COX-2

  • involved in inflammatory response
  • in macrophages, leukocytes, fibroblasts, endothelial cells (cells involved in inflammation and tissue repair)
  • produce PGI2 and PGE2
33
Q

Half-life of COX-2 selective NSAIDs tends to be _______

A

Longer half-lives, less frequent dosing (1-2 times a day)

Non-selective Naproxen is an exception - 2 times a day

34
Q

Which drug has the highest COX-1 to COX-2 inhibition ratio?

A

Ketoprofen (COX 1&raquo_space;> COX 2)

Aspirin (COX 1&raquo_space; COX 2)

Naproxen, Ibuprofen (COX 1 > COX 2)

Diclofenac, Mefenamic (COX 2 > COX 1)

Celecoxib (COX 2&raquo_space; COX 1)

Etoricoxib (COX 2&raquo_space;> COX 1)

35
Q

[Adverse effects of COX-2 inhibitors]

  • Explain the GI adverse effects compared to non-selective NSAIDs
A

COX-2 selective NSAIDs have lower risk of GI bleed

GI bleed is more of a COX-1 inhibition-dependent adverse effect, due to constitutive expression of COX-1 in the stomach

Therefore, coxibs may be more appropriate for long-term chronic conditions

HOWEVER,

  • there is dose-dependent selectivity for COX-2
  • celecoxib is the least COX-2 selective amongst COX-2 inhibitors
36
Q

[Clinical effects of COX-2 inhibitors]

  • Explain the anti-inflammatory and analgesic effects compared to non-selective NSAIDs
A

COX-2 selective NSAIDs have more anti-inflammatory and analgesic effects since inflammatory stimulus causes more COX-2 production of prostaglandins

However this is dose-dependent, non-selective NSAIDs can also achieve the same clinical effects at higher doses, but with risk of GI SEs

37
Q

[Clinical effects of COX-2 inhibitors]

  • Explain the antiplatelet compared to non-selective NSAIDs
A

COX-1 inhibition have more antiplatelet effect, especially aspirin which is an irreversible cox-inhibitor

This is not dose-dependent, aspirin achieves antiplatelet effect at low dose

38
Q

[Clinical effects of COX-2 inhibitors]

  • Explain the antipyretic effects compared to non-selective NSAIDs
A

COX-2 selective NSAIDs have poor antipyretic effects as they are relatively poor in getting into the brain (CNS) compared to non-selective NSAIDs and paracetamol

39
Q

[Unwanted effects of COX-2 inhibition]

Renal toxicity

A

COX-1 and COX-2 are both constitutively expressed in the kidney, inhibit production of PGE2, PGI2

40
Q

[Unwanted effects of COX-2 inhibition]

Reproductive issues

A

COX-2 expressed in female reproductive system

  • Effects on ovulation, including delayed follicular rupture => less likely to get pregnant

Premature closure of ductus arteriosus (fetal lung bypass) in late pregnancy

All NSAIDs are CONTRAINDICATED in 3rd trimester of pregnancy (bc all NSAIDs inhibit COX-2)

41
Q

[Unwanted effects of COX-2 inhibition]

Impaired wound healing

What are the implications?

A

Inducible COX-2 involved in inflammatory response

COX-2 involved in activation of fibroblasts and endothelial cells that are involved in tissue repair

  • COX-2 inhibition impairs wound healing
  • COX-2 inhibition exacerbates ulcers

Implications - CAUTION for use in:

  • pt with existing ulcers or other ulcer risk factors
  • post-surgical analgesia
  • concerns over non-union (defective healing) of fractures and bone repair
42
Q

[Unwanted effects of COX-2 inhibition]

Increased risk of thrombosis

A

COX-2 inhibitors cause shunting of arachidonic acid into COX-1 pathway which greatly increases the production of TXA2, resulting in platelet aggregation

=> coxibs are PROTHROMBOTIC

43
Q

What contributes to the risk of heart attack and stroke?

A
  1. Renal effects causing hypertension
  2. Risk of prothrombotic effects

Caution for use in:

  • elderly
  • hx of cerebrovascular or cardiovascular disease

Risk of MI and stroke applies for all NSAIDs except aspirin

44
Q

List the contraindications for NSAIDs use

A
  • Severe kidney impairment (eGFR <30ml/min)
  • Severe heart failure
  • Active GI ulcer or bleed
  • Bleeding disorders (e.g., hemophilia) - esp for non-selective and aspirin
  • Use of systemic corticosteroids or antiplatelet agents/anticoagulants - esp w non-selective NSAIDs
  • Multiple risk factors for NSAID toxicity (elderly w hx of GI bleed)
  • Third trimester (24-40 weeks) of pregnancy

Others (from DP)

  • Use for CABG surgery (incr risk of heart attack, stroke)
  • Severe liver impairment - child pugh C
  • Hyperkalemia
  • IBD
  • Bariatric surgery - risk of developing anastomotic ulcerations/perforations (non-selective)
45
Q

Choice of NSAID and Clinical Safety Considerations (IC16) based on risk factors/concerns:

  • Risk of renal toxicity
A

Choice of NSAID:

  • All NSAIDs a/w renal toxicity, consult doctor before prescribing

Clinical Safety Considerations (IC16):

  • Avoid non-selective and cox-2 selective NSAIDs in severe kidney impairment
  • Use with caution with diuretics and ACEi/ARB
46
Q

Choice of NSAID and Clinical Safety Considerations (IC16) based on risk factors/concerns:

  • Risk of CVD toxicity
A

Choice of NSAID:

  • Avoid cox-2 selective NSAIDs as well as Diclofenac
  • Note that celecoxib may still be used at lower doses <400mg/day
  • Use of celecoxib and ibuprofen should be limited to =<5 days
  • If cannot use celecoxib, ibuprofen, naproxen; consider paracetamol

Clinical Safety Considerations (IC16):

  • Avoid all NSAIDs in: HF, IHD, PAD, uncontrolled HTN
  • May use low dose celecoxib 200mg/day if needed

Generally, avoid in:

  • established CVD
  • uncontrolled HTN
  • significant CV risk factors: HTN, HLD, DM, smoking
47
Q

Choice of NSAID and Clinical Safety Considerations (IC16) based on risk factors/concerns:

  • Risk of GI toxicity
A

Choice of NSAID:

  • Avoid non-selective NSAIDs, use COX-2 selective NSAID with caution (but avoid if there is active GI bleed/ulcer)
  • Consider co-prescribing PPI as a GI protectant

Clinical Safety Considerations (IC16):

  • Non-selective NSAID: avoid use w anticoagulants and NSAIDs; avoid in active PUD/GI bleed
  • COX-2 inhibitors: avoid use w NSAIDs/baby aspirin; use with caution in active PUD/GI bleed (as may exacerbate existing ulcer)
48
Q

Choice of NSAID and Clinical Safety Considerations (IC16) based on risk factors/concerns:

  • Risk of NSAID-related bronchospasm and/or pseudoallergic reaction
A

Choice of NSAID:

  • Avoid non-selective NSAIDs
  • Use COX-2 selective NSAID with caution (lower risk due to less shunting into leukotriene pathway, since COX-1 pathway still available)

Clinical Safety Considerations (IC16) for NSAID-exacerbated respiratory disease (pseudo-allergy):

  • Nonselective: avoid in asthma
  • Cox-2 selective: use with caution in asthma
49
Q

Clinical Safety Considerations (IC16) for cross-sensitivity hypersensitivity reactions

A

Clinical Safety Considerations (IC16) for cross-sensitivity hypersensitivity reactions:

  • Avoid non-selective NSAIDs in hypersensitivity reactions (esp anaphylaxis/serious skin reactions) to the NSAID used or other NSAIDs including aspirin
  • Avoid COX-2 selective inhibitors in hypersensitivity reactions (esp anaphylaxis/serious skin reactions) to coxibs, aspirin, other NSAIDs, and sulfonamides (for Celecoxib)
50
Q

Advise/Counsel patients about NSAIDs

A
  • Take as prescribed
  • Use for shortest duration possible (not more than 5 days)
  • Combine NSAID with paracetamol initially, then cases NSAID and continue paracetamol only
  • Seek med advice if NSAID is still needed after 5 days
  • Not to take with food as reduces absorption rate, delays peak concentration, and reduce NSAID efficacy (may take with food to alleviate GI SEs)
51
Q

Other SEs of PO NSAIDs (IC16)

A

Effects on BP and HTN

  • monitor BP, discontinue/lower dose if BP increases
  • do not start in patient with uncontrolled HTN, risk of HTN urgency/crisis

Skin reactions

  • more likely with oxicam, sulindac, diflunisal

Hematologic effects

  • bleeding risk due to inhibition of platelet function; stop 3 days prior to surgery (1 week for aspirin)

CNS complaints

  • not common (no need to counsel)
  • ???? drowsiness, dizziness, headaches, tinnitus
52
Q

Monitoring parameters

A
  • Therapeutic response (pain, range of motion, ADL)
  • CBC and basic metabolic panel
  • Hemoglobin/Hematocrit
  • Hepatic and renal function
  • Blood pressure
  • SEs
53
Q

Topical NSAIDs counseling on SEs:

A
  • Mild redness and skin irritation in the area on which the medication is applied
  • Sensitivity to UV ray such as sunlight (itching, swelling and blistering of the skin following sun exposure)

3154 MSK (12 decks)

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