Inflammation - 1 of 5 Pain

#KYJ - Inflammation pain

Episode 1 of 5

In KYJ (#KnowingYourJargon) we explore those terms in health that we use commonly, yet often don't understand.

Think of KYJs as putting the science into your nursing artistry.

Inflammation

It starts with tissue damage and involves a storm of cellular chemicals that have 5 cardinal effects.

Dolor = Pain

Calor = heat

Rubor = Redness

Tumor = swelling

Loss of function = doesn't rhyme with the other four.

So let's look at why we see these symptoms.  In this episode- Pain

Pain is thought to be through multiple mechanisms.

Pain receptors (nociceptors) in your tissues fall loosely into two categories. 

Fast Delta-A fibres transmit sharp, burning pain messages to the spinal cord and brain for processing.

Slow C fibres transmit the dull ache of pressure/crushing, heaviness.  Pulsatile throbbing and crampy pain.

Both are stimulated directly by chemicals released during injury, but both are also stimulated by delayed manufacture of inflammatory chemicals made by the immune system eg bradykinin, and prostaglandins.

To start to understand inflammatory pain, let's explore what happens at the site of injury.  A cut or splinter.

Direct skin cell injury causes destruction of the membranes that encapsulate cells.  This membrane you will remember from grade 9 science, is made of fat (lipids).  It is actually a phospholipid that you know better by its common name Cholesterol.

That's right, all cells are lined by cholesterol and our liver makes this constantly to build cells and repair dead tissue.

But that is a whole other post.

So ... Cells are damaged, the phospholipid membrane leaks into the interstitial fluids (Extracellular fluid) around all our cells.

An enzyme present in this fluid is called Phospholipase (foss-foe-lype-aze). Any enzyme you read about inside our bodies will end with the suffix "-ase".

Now this enzyme breaks down the phospholipids released during injury, and it converts them into an acid called Arachidonic Acid.

Another enzyme present in extracellular fluid called cyclooxygenase or COX for short , now acts on the newly created Arachidonic acid, and converts it into a pro-inflammation protein called prostaglandin.

Many prostaglandins are responsible for stimulating those pain receptors, hence pain.

Application.  Recognising pain is chemically induced by this injury cocktail of substances, let's briefly look at the two big families of anti-inflammatory drugs used for inflammatory pain.

Remember pain is stimulated by the ultimate production of prostaglandins.

Steroid drugs 

These include hydrocortisone, methylprednisolone , Dexamethasone, fluticisone, betamethasone, Prednisolone, and others you are likely familiar with.

These "sone" steroid drugs stop Phospholipase from converting phospholipid into Arachidonic acid.  This stops further stages of inflammation occuring... Including pain.

The other family of drugs is the Non steroidal antiinflammatory drugs.

Abbreviated to NSAIDs, these drugs include ibuprofen, nurofen, aspirin, indocid, naproxen, diclofenac (voltaren).

These drugs inhibit the COX enzyme converting Arachidonic acid into prostaglandins that cause inflammation and pain.

Are we done?   Questions ?

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