Pain Mangement Neuro Flashcards

1
Q

Somatic p💊

A

injury to tissues, well localized

Most analgesics will help, if severe, needs a potent analgesia

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2
Q

Visceral p💊

A

injury to organs (stretch receptors), poorly localized

Potent pain analgesia

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3
Q

Bone o 💊

A

Potent pain meds, opiates with NSAIDS as adjunct

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4
Q

Neuropathic pain 💊

A

The nervous system itself damaged, to plexuses, spinal cord. May not respond as well to usual analgesics including opioids

eg trigeminal neuralgia, DM neuropathy

Opiates + tricyclic antidepressants or other adjuvant

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5
Q

Mixed pain (nociceptive + neuropathic)

A

a- Hyperalgesia (an increased amount of pain associated with a mild noxious stimulus)

b- Allodynia (pain evoked by a non-noxious stimulus)

c- Breakthrough pain

Is it new incident (new cause? or end-of-dose?). Use 10% of total daily dose (rounded up) up to q 1-2 h

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6
Q

1.Weak COX2 selective

A

diclofenac

piroxicam)
♥️Main therapeutic effects achieved via COX-2 inhibition
⬆️ CVS risk

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7
Q

2.Moderate COX2 selective

A

celecoxib

⬆️ CVS risk

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8
Q

3.Weak COX1 selective

A

aspirin, ibuprofen, naproxen

👾👾Cox 1 found in the stomach, kidney ,platelets ➡️nephrotoxic,ulcer ,anti platelets

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9
Q

4.Highly COX1 selective

A

ketorolac
Nephrotoxic
👾👾Cox 1 found in the stomach, kidney ,platelets ➡️nephrotoxic,ulcer ,anti platelets

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10
Q

Partial agonists opoids

A

Morphine is a partial agonist at μR similar to pethidine.

Codeine and tramadol are weak agonists

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11
Q
  1. Pure agonists. uR
A

Peptides eg endorphin: Non-peptides such as Fentanyl, and methadone.

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12
Q

Antagonists of opoids

A

Naloxone and naltrexone

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13
Q

Neuropathic pain relieving drugs 💊

A
Opoids+
Anticonvulsant 
gabapentin, carbamazepine
Anti-depressent
Ssri
Tca
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14
Q

1.Paracetamol👾👾

A

had only mild analgesic and antipyretic effect

1- inhibits COX3 varient of COX1

2- Inhibits low rate of COX2

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15
Q

Opoids use

A

:

1- Severe pain eg postoperative, cancer

2- Acute heart failure

3- Antidiarrheal

4- Antitussive

5- Refractory migraine

6- treatment of addiction

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16
Q

Instructions and monitoring of effect/toxicity outcomes by NSAIDs

A

1- Taken on full stomach

3- Regular check of BP

4- Skin rash monitoring especially mefenamic, (urticuria, SJS)

5- Blood film monitoring monthly

6- Bronchospasm and bleeding time except COX2 inhibitors

7- Renal function test if prolonged time (eg paracetamol)

2- Epigastric pain monitoring,tarry stool

Causation of NSAIDs gastric ulcer in sequence

Ketoprofen > piroxicam > naproxen > diclofenac > aspirin > fenoprofen

17
Q

Neuronal Membrane stabilizers

A
  • Ketamine, a dissociative anaesthesia
  • Memantine blocks NMDA receptors in dorsal horn
  • Ziconotide, blocks N-type Ca ch analgesic agents.
18
Q

Local anesthesia

A

1- Wound infiltration: 2 % lidocaine ( +/- adrenaline)

2- Nerve blocking: specific nerve distribution eg femoral nerve block

Advantages:

1- Excellent analgesia. 2- No sedation.

Complications

1- Bleeding, 2-Horners syndrome, 3- infection, 4-nerve injury,

5- spreeding of local anesthetic drug, 6- vascular injury, 7pneumothorax(according to the site of process