Pharmacology of non-narcotis analgesics Part 2 Flashcards Preview

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Flashcards in Pharmacology of non-narcotis analgesics Part 2 Deck (12):

what is neuropathic pain?

Results from injury to the peripheral or central sensory nerves due to:
Endocrine disease: diabetes mellitus
Connective tissue disease: Rheumatoid Arthritis
Viral infection:
Herpes zoster or Shingles (post herpetic neuralgia)
HIV neuropathy
Chemotoxicity: cancer chemotherapy
Different from nociceptive pain caused by tissue damage releasing chemical pain mediators


what are neuropathic pain characteristics?

Hyperalgesia: Increased pain evoked by noxious stimulus
Allodynia (allo: other, dynia:pain): pain caused by stimuli that are not normally painful: touch or bedclothes, wind
Paresthesias: tingling, pins and needles,
Dysesthesias: burning, shooting, electric shock-like sensation


what is the pathophysiology of non-narcotic analgesics?

The primary afferent neurons are hyperactive discharging spontaneously
Over time the neuron in dorsal root ganglia and dorsal spinal horn change:
↑ Expression of Na+ channels
→ Na+ channel blockers: Carbamazepine and Lamotrigine help
→ Ca2+ channel blockers alpha 2 delta subunit (prevent release of several neurotransmitters: Pregabalin, Gabapentin
Blockade of serotonin and
norepinephrine reuptake
→ Tricyclic antidepressants
- Nortriptyline, Amitriptyline
→ Other serotonin reuptake inhibitors
- Duloxetine
- Venlafaxine


what are the treatment general principles?

A stepwise approach is recommended
Start with one of the first-line agents
Allow sufficient time for response (several weeks of treatment may be required for full response)
If some response to lower dose, titrate to the max dose
If inadequate response despite adequate trial, switch to another first-line agent.
If partial response to adequate dose of first medication, may add a second first-line agent.
If inadequate response to 2 first-line medications, may add narcotic analgesics or local Lidocaine injection.


what is trigeminal neuralgia?

Disabling neuropathic shooting pain in the distribution of trigeminal nerve (face)
Trigger zones:
Chewing, brushing teeth, blowing wind to face
Younger patients: rule out demyelination--multiple sclerosis
Older patients: a pulsating vascular loop touching the trigeminal nerve causing demyelination
MRI brain and MRI with angiogram is important
Na+ channel blocker antiepileptic drugs are helpful
If no response to AEDs, surgery for vascular loop decompression or transcutaneous trigeminal nerve glycerol injection (rhizotomy) are other options.


what is fibromyalgia?

Chronic diffuse pain (18 tender points) & allodynia + ↑ painful response
to pressure
↑ sensitivity of brain to pain signals due to ↓ pain threshold
Called “central sensitization”
Also may have fatigue, sleep disturbance and depression
Results from:
Alteration of neurotransmitters
↑ sensitivity of pain receptors triggered by repeated stimulation.
Anticonvulsant Pregabalin: FDA approved in 2007
Also Amitriptyline (tricyclic antidepressant) is used
Muscle relaxant Cyclobenzaprine (A tricyclic antidepressant, relieves central muscle tone)


what is gout?

Inflammatory joint disease caused by:
Increased uric acid in the blood and deposition of uric acid crystals in joints
Uric acid is a waste generated from purine catabolism
Normally dissolved in blood and excreted by the kidneys
If ↑ formation or ↓ excretion → precipitation where temperature is lower (distal joints)

The abnormal crystal in the joint attracts leukocytes
Attempt to phagocytose → ↑ inflammatory mediators → joint damage

Classic gout involves the big toe (Podagra)
It is more common in men 0.6% than women 0.1%, attack starts at night when body temp is ↓
Very painful, touch of bedclothes precipitates severe pain
Also painless precipitations (Tophi) in cold distal body parts (ear helix)
Several pharmacological classes are used to treat gout attacks.


how is gout treated?

Acute attack treatment goal: ↓ inflammation
NSAIDs and Corticosteroids (prednisone): ↓ inflammation by ↓ prostanoids
Cholchicine: ↓ inflammation and phagocytosis by ↓ leukocytes migration via microtubules disaggregation
Long-term treatment:
↓Uric acid → Allopurinol (a purine hypoxanthine
analog) blocks the
enzyme hypoxanthine

May use medications to increase kidney excretion

Normally 90% Urate is reabsorbed by renal tubes and only 10% is excreted.

Probenecid and Sulfinpyrazone
↑ Urate excretion by the kidney
They compete with Uric Acid for absorption via renal tubular acid transporter →↓ Urate resorbed


what are the two types of migraines?

Common Migraine
A neurovascular headache
Fulfilling criteria in table 1.1
Classic Migraine (with Aura)
Same as above plus
At least 2 episodes of aura
Aura: fully reversible sensory symptoms: visual, olfactory or difficulty of speech lasting between 5-60 minutes

look at this table in the notes


what is the treatment for migraines?

Ibuprofen: attenuate the neuroinflammation by blocking COX II

Triptans (Sumatriptan-Imitrex)
Serotonin 5HT1B/D agonists
Effective when taken early in an attack
Cause direct intracranial small blood vessel constriction
Contraindicated in:
Coronary artery disease, cerebrovascular disease
Pregnancy, breast feeding
Hemiplegic migraine
Do not combination with SSRIs → too much serotonin (serotonin syndrome)


what do ergot derivatives do for migraines?

Ergot derivatives:
Ergotamine or dihydroergotamine
May cause direct vasoconstriction
Again contraindicated in coronary artery disease
Long-term use causes retroperitoneal fibrosis (ureteral obstruction), or heart valve fibrosis (valve dysfunction)


what do you do for migraine prophylaxis?

If present > 15 days / month needs prophylaxis

Several classes of medications are used:
Beta blockers: Propranolol
Tricyclic antidepressants: Nortriptyline
Voltage gated calcium channel blocker: Verapamil
Antiepileptic drugs: Topiramate