P5 PHARMACOLOGY Flashcards

Pharmacology of osteoarthritis

1
Q

examples of topical NSAIDs

A

methyl saIicyIate cream
DiethyIamine saIicyIate (LIoyd’s cream)
DicIofenac cream
Topical capsaicin

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2
Q

Examples of intra-articular glucocorticoid injections

A

TriamcinoIone acetonide
MethyIprednisoIone acetate

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3
Q

Maximum dose of paracetamol

A

4 gm/day

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4
Q

OD of paracetamol can cause

A

acute liver failure

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5
Q

MOAs of oral NSAIDs

A
  • non selective COX-1 & COX2 inhibitors
  • selective COX2 inhibitors
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6
Q

common example of opioid analgesic

A

tramadol

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7
Q

oral NSAIDs should be co-prescribed with

A

PPIs / H2 receptor inhibitor

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8
Q

reactive intermediate in paracetamol metabolism that in OD can lead to liver failure

A

NAPQI=N-acetyIe-para-benzoquinone imine

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9
Q

LEVELS of arachidonic acid & peroxidase in broken cells

A

both high

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10
Q

LEVELS of arachidonic acid & peroxidase in normal intact cells

A

both low

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11
Q

Intermediate in acetaminophen metabolism that crosses BBB

A

p-aminophenol

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12
Q

Mechanism in which AM404 activates CB1 receptors

A

by inhibition of anandamide re-uptake

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13
Q

CB1 & TRPV1 are involved in transmission and modulation of

A

pain

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14
Q

PH levels in inflammation

A

high Ph

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15
Q

strongly recommended intervention for knee & hip osteoarthritis

A

intra-articular glucocorticoid injection

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16
Q

indications for IAGC use

A
  • Severely inflamed large monoarthritis
  • unresponsive to NSAIDs
  • intolerance to NSAIDs
17
Q

Glucocorticoids Preparations

A

1- non-ester preparations
2- ester preparations

18
Q

enzyme that is needed to hydrolase ester preparations

A

Cellular esterases

19
Q

Examples of steroid injections

A
  • methylprednisolone acetate
  • dexamethasone acetate
    -dexamethasone sodium
19
Q

adverse effects of IACG

A

Infection
capsular calcification
tendon rupture
cutaneous atrophy
post injection flare
Osteonecrosis

19
Q

Absolute contraindication for corticosteroid injections

A
  • local / intra-articular sepsis
  • bacteremia
  • intra-articular fracture
  • joint instability
20
Q

factors affecting systemic absorption of anaesthetic

A
  • dosage
  • vasodilating properties
  • presence of vasoconstrictor agent
  • nature of administration site
  • drug-tissue binding
21
Q

Vasoconstrictor agents

A

adrenaIine
NoradrenaIine
FeIypressin

22
Q

vasodilating agents that has the highest vasodilating properties

A

bupivacaine
etidocaine

23
advantages of vasoconstrictor agents while administrating anaesthesia
- Prolong & increase the depth of anaesthesia - reduce or Limit the systematic toxicity -render the area of injection Iess hemorrhagic
24
Mechanism in which vasoconstrictors reduce the systemic toxicity
by delaying its absorption into generaI circulation
25
order of loss of sensation in anaesthesia
pain Temperature touch Pressure
26
order of nerve block
-SmaII myeIinated fibers -SmaII unmyeIinated fibers Large myeIinated fibers Large unmyeIinated fibers
27
biotransformation of amino esters is done by
plasma pseudocholinesterase
28
amino esters Systemic Toxicity is more likely to occur in
Individuals with genetically determined pseudochoIinesterase deficiency
29
amino esters hypersensitivity reactions are more likely due to formation of
PABA = para-aminobenzoic acid
30
biotransformation of amino amides is done by
Iiver (Cytochrome P 450)
31
amino amides Systemic Toxicity is more likely to occur in
individuaIs with hepatic diseases, reduction in hepatic bIood fIow (due to heart faiIure, β-bIockers), hepatic enzyme inhibitors