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PR3154 FINALS > Analgesics + Soft Tissue Injuries > Flashcards

Analgesics + Soft Tissue Injuries Flashcards

1
Q

What kind of NSAID is aspirin?

A

non-selective irreversible

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2
Q

What kind of NSAIDs are ibuprofen, naproxen and diclofenac?

A

non-selective reversible

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3
Q

What kind of NSAIDs are celecoxib, parecoxib and etoricoxib?

A

COX-2 selective

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4
Q

What kind of analgesic is paracetamol?

A

CNS-selective reversible COX-inhibitor

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5
Q

What are the opioid drugs?

A

mild: tramadol, codeine
strong: morphine, oxycodone, fentanyl

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6
Q

Cell membrane phospholipids are acted on by phospholipase A2 to form arachidonic acid. What 3 products are formed from AA and what are the enzymes used?

A
  1. Lipoxins (by 15-lipoxygenase)
  2. Prostanoids (by COX)
  3. Leukotrienes (by 5-lipoxygenase)
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7
Q

What are lipoxins, prostanoids and leukotrienes called collectively?

A

Eiconsanoids

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8
Q

Which types of inflammation are prostanoids and leukotrienes more selective for respectively?

A

prostanoids - acute inflammation
leukotrienes - chronic inflammation (and immune response)

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9
Q

Which enzymes do steroids and NSAIDs inhibit respectively?

A

steroids - phosphilipase A2 (affects all eicosanoids)
NSAIDs - cox (affects prostanoids)

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10
Q

What are 3 prostaglandins inhibited by NSAIDs?

A

PGI1 - prostacyclin
PGE2 - classical prostaglandins
TXA2 - thromboxanes

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11
Q

What are the effects of PGI2, PGE2 and TXA2?

A
  • Prostacyclins (PGI2) → vasodilation (in closed wound); inhibition of platelet aggregation
  • Classical prostaglandins (PGE2) → vasodilation or vasoconstriction; vascular permeability (edema); pain
  • Thromboxanes (TXA2) → vasoconstriction (in open wound, thrombosis); platelet aggregation
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12
Q

Which 2 prostaglandins does aspirin block? What are the 3 physiological effects of this blockage?

A

PGE2 PGI2

  1. blocks vasodilation (hence less heat redness swelling)
  2. increases vasc permeability (hence less swelling)
  3. decreases pain
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13
Q

Explain why aspirin has an analgesic ceiling?

A

It blocks the production of prostaglandins, which sensitises the nociceptive fibres to stimulation by other inflammatory mediators

PG effect may already be turned off to the maximum but other signalling chemicals (eg. ATP, bradykinins, leukotrienes, K+) are still there

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14
Q

How do typical NSAIDs (eg. aspirin) exert CNS effect?

A

In infection, neutrophils increase IL-1 synthesis in the brain, which increases COX expression in the hypothalamus

This increases PGE2 levels resulting in fever

NSIADs that cross the BBB inhibit brain COX hence decreasing PGE2 in the brain and decreasing fever

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15
Q

What are the side effects of aspirin? (6)

A
  1. Reyes syndrome
  2. GI side effects
  3. Renal side effects
  4. Asthma
  5. Allergy/pseudoallergy
  6. Bleeding
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16
Q

What is Reye’s syndrome and what increases its risk?

A

Encephalitis and liver swelling
sx: vomiting, personality changes, listlessness, delirium, convulsions, loss of consciousness

increased risk in kids w viral infection, CI in children

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17
Q

What is the recommended duration of NSAID use to minimise GI SE?

A

Max 5 days

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18
Q

How do renal side effects arise?

A

Blockage of PGE2 and PGI2 in the kidneys, alters renal blood flow dynamics

PGE2 inhibits Na+ reabsorption at the TAL (25% reabs) → sodium retention, water retention, peripheral edema, HTN

PGI2 stimulates the secretion of renin and therefore aldosterone → hyperkalemia and acute renal failure

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19
Q

NSAIDs should be used with caution in patients with HTN or at risk of renal failure. What is triple whammy therapy?

A

NSAIDs, diuretics and ACEis
(NDA)

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20
Q

What are the risk factors for NSAID-induced AKI

A

old age, chronic HTN, atherosclerosis, pre-existing glomerular disease or renal insufficiency, volume depletion, cirrhosis or HF, use of ACEi or ARBs, use of triple whammy

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21
Q

Which mediator can trigger bronchospasms?

A

Leukotrienes

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22
Q

What is the sensitivity triad?

A

Asthma, chronic urticaria and nasal polyps

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23
Q

Will switching to another NSAID (with a different chemical structure) be helpful in pseudoallergy?

A

May not be effective as the pt is sensitive to COX inhibition and the rxn is not from antibodies against the chemical structure

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24
Q

What are 3 other typical NSAIDs and their important learning points?

A
  1. Naproxen - higher free fraction in women
  2. Indomethacin - strong (phospholipase A inhibition) but CNS SE
  3. Diclofenac - short half life and therefore low GI risk but gd for joint disease
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25
Q

Differentiate between COX1 and COX2 and how they contribute to side effects?

A

COX-1 is constitutive and usually results in “housekeeping” functions
COX-2 is inducible and usually causes inflammation

Most adverse effects come from the inhibition of COX-1 and therefore the inhibition of normal housekeeping functions

Selection of COX-2 over COX-1 (both produce PGI2 and PGE2) helps reduce GI and bleeding effects, but does not spare the patient from renal effects

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26
Q

What are the side effects of COX2 inhibitors? (5)

A
  1. Renal toxicity
  2. Effects on ovulation
  3. GI side effects
  4. Thrombosis risk
  5. Increased CV risk
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27
Q

Why is there higher thrombosis risk with COX-2 selective NSAIDs?

A

relative increase in TXA2 to PGI2 (produced by COX-1), which favours platelet aggregation, which may increase the risk of thrombosis

28
Q

What are contraindications to NSAID use? (7)

KHABD MP

A
  1. Severe kidney impairment (eGFR < 30ml/min)
  2. Severe HF
  3. Active GI ulcer or bleed
  4. Bleeding disorders (eg. hemophilia)
  5. Use of systemic corticosteroids or antiplatelet agents or anticoagulants
  6. Multiple risk factors for NSAID toxicity (eg. elderly with hx of GI bleed)
  7. Third trimester of pregnancy

KHABD MP

29
Q

In risk for CV toxicity, which drugs are preferred and which shouldn’t be used?

A

Use: celecoxib, ibuprofen (< 5d)
Don’t use: diclofenac

30
Q

In risk for GI toxicity and asthma/allergy, which drugs are preferred and which shouldn’t be used?

A

Use: celecoxib (add PPI)
Don’t use: ibuprofen (non-selective)

31
Q

What are the advantages of paracetamol? (6)

A
  • good analgesic
  • potent antipyretic
  • spares the GI tract
  • side effects are few and uncommon
  • few drug interactions
  • relatively safe for pediatric use
32
Q

What are the disadvantages of paracetamol? (3)

A
  • weak anti-inflammatory (only addresses pain, not the cause)
  • toxic doses cause nausea, vomiting and liver damage
  • and allergic skin reactions can sometimes occur
33
Q

What are cautions and overdoses with paracetamol?

A

Caution: pts with hepatic dysfunction or alcohol abuse

Overdoses can lead to liver damage and patients who OD should be referred to ED if ≥ 10g per 24h
Higher risk of harm with doses ≥ 4h per 24h

34
Q

When should paracetamol dose be reduced

A

overweightness can cause AKI risk factors

35
Q

How should paracetamol and ibuprofen be taken for stronger for longer effect?

A

Together (not alternate)

36
Q

What is the advantage of opioids over NSAIDs

A

analgesic effect increases as opioid dose increases (no ceiling)

37
Q

Which opioid response varies greatly between individuals and why?

A

Codeine
Part of codeine (0-15%) is transformed to morphine in the body, depending on CYP2D6 polymorphisms

38
Q

What are side effects of opioids

A

GI effects (constipation, nausea, vomiting), sedation and drowsiness (resulting in accidents), hormonal effects, depression, respiratory effects, tolerance, physical dependence, addiction and/or withdrawal, opioid-induced hyperalgesia, falls and fractures (especially in elderly) and overdose and death

39
Q

What are 6 risk factors with opioid use?

A
  1. Combination with other CNS depressants → worsens sedation
  2. Other co-morbidities (eg. mental health conditions)
  3. Renal or hepatic insufficiency, age > 65 yo
  4. Pregnancy (risk to both mother and fetus)
  5. Personal or family history of substance use disorder
  6. Already prescribed with an opioid (increased risk with increased dose and duration of use, risk of diversion and opioid use disorder)
40
Q

What are causes of pain? (5)

A

IMPT: periparticular pain
others: referred visceral pain, bone pain, tissue pain, neuropathic pain

41
Q

What are the features of periarticular pain? (3)

A
  • more pain on active movement than passive movement
  • maximal pain in certain lines of muscle pull
  • point of maximal tenderness is not at the joint line on palpitation
42
Q

Which soft tissue injuries warrant urgent ED referral? (LLIM)

A

ligament fracture
lower back pain relating to underlying visceral causes
infection-related causes
malignancy or metastasis (lower back pain)

43
Q

What does RICER stand for

A

Rest, Ice, Compression, Elevation, Referral

44
Q

How should icing be done

A
  • Icing can be done using an ice pack or compression spray which cool the skin and help induce vasoconstriction, hence reducing the transport of inflammatory mediators
  • This should be done no longer than 15 minutes with no direct skin contact which might burn the skin
45
Q

What does NO-HARM stand for

A

No Heat, Alcohol, Re-injury, Massage

46
Q

What are the 4 main types of soft tissue injuries and what types of tissues do they refer to?

A
  • Sprains (bone-to-bone connective tissue) → ligament
  • Tendonitis (muscle-to-bone connective tissue) → tendon
  • Bursitis (fluid-filled sacs around joints that cushion tendons or muscles from adjacent bones) → inflammation of bursae
  • Plantar fasciitis (fibrous attachment connecting heel bone to base of toes) → inflammation of the plantar fascia
47
Q

What is the most common type of sprain? What is usually observed with sprains?

A

lateral ankle sprains, which is caused by an inversion of the foot and is usually sustained during sport activities

There is a sudden onset of pain and swelling after the “pop” sound

48
Q

What warrants referral to ED in sprains?

A

Cannot bear weight

49
Q

What are the 3 features of tendonitis?

A

local pain and dysfunction
inflammation
degeneration

50
Q

What are the 5 etiological causes of tendonitis? (DISCO)

A

drug induced (FQ and statins)
inflammatory rheumatic disease
sports injury
calcium apatite deposition (from metabolic disturbances)
overuse (repeated mechanical loading)

51
Q

What is a bursae and when does pain occur in bursitis?

A

fluid-filled sac-like structure lined by synovial membrane in clefts between mobile structures

when motion compresses adjacent bursa to the point where intrabursal pressure increases (eg. fully flexed elbow)

52
Q

Compare between acute and chronic bursitis (features and etiology)

A
  • Acute bursitis (more pain): trauma/injury, crystal-induced process (eg. gouty bursitis), infection (eg, septic bursitis)
  • Chronic bursitis (less pain, more swelling): overuse, prolonged pressure (eg. kneeling or leaning), inflammatory arthritis (eg. RA)
53
Q

What are the 4 classes of causes for plantar fasciitis

A

neurologic causes
skeletal causes
soft tissue causes
inflammatory disorders

54
Q

What are red flags with respect to neurological causes in plantar fasciitis?

A

paresthesia, nocturnal sx, pain from posterior leg to heel

55
Q

What are red flags with respect to skeletal causes in plantar fasciitis?

A

trauma, fever, constant pain, nocturnal sx

56
Q

What are red flags with respect to inflammatory disorder causes in plantar fasciitis?

A

PMH/FH of inflammatory disorder, erythema nodosum

57
Q

Describe the presentation of adhesive capsulitis

A

unilaterally (usually non-dominant side, but other side may also be affected within 5 years), with limited reaching overhead, to the side, across the chest and limited rotation

58
Q

Briefly describe the 3 stages of adhesive capsulitis

A
  • Initial (2-9 months): severe disabling shoulder pain, worse at night, increasing stiffness
  • Intermediate (4-12 months): stiffness and severe loss of shoulder motion, pain gradually lessens
  • Recovery phase (5-24 months): gradual return of range of motion
59
Q

When should adhesive capsulitis be referred to a specialist?

A

if marked loss of motion is present

60
Q

How should adhesive capsulitis be managed? (3)

A
  • Analgesics for pain (paracetamol, NSAIDs, weak opioids)
  • Range of motion exercises
  • Intraarticular glucocorticoid + physical therapy
61
Q

What are reasons for referral for lower back pain and their respective causes? (2+3+1)

A

Mechanical causes
- Spinal cord compression (neuro sx)
- OP # (chronic GC use, age, trauma)

Nonmechanical causes
- Malignancy (unexplained weight loss)
- Spinal fluid infection (fever, recent spinal inj, immunocomp)
- Osteomyelitis (fever, constant pain)

Visceral
- severe abdominal pain

62
Q

How should acute and subacute lower back pain be treated?

A
  • Non-pharmacological measures
  • NSAIDs or skeletal muscle relaxants
63
Q

How should chronic lower back pain be treated?

A
  • Non-pharmacological measures including exercise
  • NSAIDs as a first line, or alternatively tramadol or duloxetine
64
Q

List 6 NPM for lower back pain

A
  1. Engage in low-impact core strengthening exercises to improve spine stability
  2. Use correct lifting and moving techniques
  3. Maintain correct posture when sitting or standing
  4. Quit smoking
  5. Avoid stressful situations
  6. Maintain a healthy weight
65
Q

What are symptoms of myalgia that warrant an urgent referral to the ED? (2 classes)

A

Infection-related (especially bacterial) → endocarditis and impending sepsis presenting with fever, chills and back pain

Medication toxicity → muscle pain, muscle weakness, tea-coloured urine (from statins, ciprofloxacin, bisphosphonates)

66
Q

What are SAMS symptoms?

A

proximal symmetric muscle weakness and/or weakness of the hips, thighs, calves and rarely arms

67
Q

What are 2 important counselling points for SAMS?

A
  • Statins should be discontinued if CK > 10X ULN with or without unexplained muscle symptoms
  • Advice drinking large quantities of fluids to facilitate the renal excretion of myoglobin to prevent renal failure

PR3154 FINALS (6 decks)

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