Physiology of Low Back Pain and Pharmacological Actions of NSAIDs

ASSIGNMENT -1
1. Explain the physiology of low back pain.
Pain is a subjective, physical and emotional unpleasant sensation caused due to tissue
damage as a result of an illness or injury. Lower back pain (LBP) is fifth most common
and affects two-third of the population at some point in their lives. Pain can be classified
according to their duration as acute (lasting less than six weeks), sub-chronic(lasting from
6-12 weeks) and chronic (lasts more than 12 weeks). The specific etiology of pain is
uncertain although it may arise due to mechanical trauma to muscle or joint, non
mechanical means or may be referred. Acute lower back pain may arise from twisting,
bending or lifting heavy. It may result in pin point or diffuse tenderness accompanied
with mild pain, uneasiness, deprived sleep and depression. (Bogduk, 2009)
Lower back has five vertebrae L1-L5 including sacrum. A fibro cartilagenous disc acts as
a cushion and prevent rubbing of these vertebrae. Muscles and ligaments of back and
abdomen support and protect the spine. Multifidus muscles are responsible for keeping
spine stable during movements. In patients with chronic back pain malfunctioning of
these muscles are found which persist even after the pain has been subsided. This may be
the case with Sue.
The intervertebral disc is composed of a gelatinous core which is surrounded by a fibrous
disc. These structures are devoid of nerve and blood supply. With continuous wearing
these discs lose their ability to absorb forces and flexibility which puts pressure on the
spine resulting in thickening of the ligaments and development of bony overgrowth on
the vertebrae which reduces the space available for vessels to pass through them and
hence they grow from the interior putting pressure on the nerve root resulting in
development of pain. (Moseley, 2004)

2. Discuss pharmacological actions and effects of NSAIDs
Non- steroidal anti-inflammatory drugs are analgesic medicines widely prescribed to
achieve relieve from pain and inflammation. They are also advised to patients with fever
as it brings down the body temperature. (Vane, 2000)
NSAIDs mainly show anti-inflammatory and analgesic effects. These are enzyme
inhibitors that act primarily on cyclo-oxygenase (COX) which is an enzyme responsible
for production of prostaglandins. Prostaglandins are mediators of inflammation that are
known to sensitize the peripheral nociceptors i.e. nerve receptors. NSAIDs decrease the
concentration of prostaglandins to provide a combined effect of anti-inflammatory and
analgesic action. Cyclo-oxygenase are found in two forms as COX-1 and COX-2. COX-1
is potentially found in all tissues of the body which catalyzes the formation of
prostaglandins. On the other hand COX-2 is formed in damaged and inflamed cells and
hence inhibition of these provides a decrease in production of prostaglandins which
provides an analgesic, antipyretic and anti-inflammatory action. Inhibition of COX-1 can
lead to unwanted physiologic changes like gastric ulceration, renal complications.
However, apart from peripheral inhibition of prostaglandins, NSAIDs provide analgesic
action through various other mechanisms (central and peripheral).
Another mechanism is by inhibition of neutrophil function by NSAIDs which impedes
the activities of enzymes which results in providing relief from inflammation.
Some NSAIDs may also be unable to block lipooxygenase pathway that produces
inflammatory reaction.
Adverse effects of use of these drugs include headache, blurred vision, salicylism, cardiac
complications, nausea, vomiting. Peptic bleeding and ulceration is commonly found. It
may also lead to bronchial asthma, rashes, renal insufficiency and faliure, depressed
respiration. Use of NSAIDs is contraindicated in patients suffering from peptic ulcer,
broncial asthma, and allergy (Weir, 2002)

REFRENCES
Burian, M. and Geisslinger, G., 2005. COX-dependent mechanisms involved in the
antinociceptive action of NSAIDs at central and peripheral sites. Pharmacology &
therapeutics, 107(2), pp.139-154.
Bogduk, N., 2009. On the definitions and physiology of back pain, referred pain, and
radicular pain. Pain, 147(1-2-3), pp.17-19.
Forst, S.L., Wheeler, M.T., Fortin, J.D. and Vilensky, J.A., 2006. The sacroiliac joint:
anatomy, physiology and clinical significance. Pain physician, 9(1), pp.61-67.
Oddsson, L.I. and De Luca, C.J., 2003. Activation imbalances in lumbar spine muscles in
the presence of chronic low back pain. Journal of applied physiology, 94(4), pp.1410-
1420.
Moseley, G.L., 2004. Evidence for a direct relationship between cognitive and physical
change during an education intervention in people with chronic low back pain. European
Journal of Pain, 8(1), pp.39-45.
Sostres, C., Gargallo, C.J., Arroyo, M.T. and Lanas, A., 2010. Adverse effects of non-
steroidal anti-inflammatory drugs (NSAIDs, aspirin and coxibs) on upper gastrointestinal
tract. Best practice & research Clinical gastroenterology, 24(2), pp.121-132.
Suleyman, H., Halici, Z., Cadirci, E., Hacimuftuoglu, A. and Bilen, H., 2008. Indirect
role of beta2-adrenergic receptors in the mechanism of anti-inflammatory action of
NSAIDS. J Physiol Pharmacol, 59(4), pp.661-672.
Vane, J.R., 2000. The mechanism of action of anti-inflammatory drugs. In Advances in
eicosanoid research (pp. 1-23). Springer, Berlin, Heidelberg.
Weir, M.R., 2002. Renal effects of nonselective NSAIDs and coxibs. Cleveland Clinic

journal of medicine, 69(1), pp.53-58.