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
Q

advantages of vasoconstrictor agents while administrating anaesthesia

A
  • Prolong & increase the depth of anaesthesia
  • reduce or Limit the systematic toxicity
    -render the area of injection Iess hemorrhagic
24
Q

Mechanism in which vasoconstrictors reduce the systemic toxicity

A

by delaying its absorption into generaI circulation

25
Q

order of loss of sensation in anaesthesia

A

pain
Temperature
touch
Pressure

26
Q

order of nerve block

A

-SmaII myeIinated fibers
-SmaII unmyeIinated fibers
Large myeIinated fibers
Large unmyeIinated fibers

27
Q

biotransformation of amino esters is done by

A

plasma pseudocholinesterase

28
Q

amino esters Systemic Toxicity
is more likely to occur in

A

Individuals with genetically determined pseudochoIinesterase deficiency

29
Q

amino esters hypersensitivity reactions are more likely due to formation of

A

PABA = para-aminobenzoic acid

30
Q

biotransformation of amino amides is done by

A

Iiver (Cytochrome P 450)

31
Q

amino amides Systemic Toxicity
is more likely to occur in

A

individuaIs with hepatic diseases, reduction in hepatic bIood fIow (due to heart faiIure, β-bIockers), hepatic enzyme inhibitors