The Lab / Core medicine / Lesson 18
When a cell is hurt, it snips a fatty tail out of its own skin and turns it into a burst of signals: some protect you, some bring pain, swelling and fever. Build that pathway one piece at a time, then watch five kinds of anti-inflammatory drugs block it, each in a different place.
Educational, not for clinical use
Build the idea
Your body is built from cells, tiny living units. Each cell is wrapped in a thin skin, its membrane. The membrane is made of phospholipids: fat molecules with a water-loving head and two oily tails, packed side by side in a double layer.
Build the idea
When part of the body is hurt by a knock, a cut or germs, it answers with inflammation: the area turns red, warm, swollen and painful. Inflammation brings help to clear the damage, and it starts with signals made from the membrane itself.
Build the idea
Injury switches on an enzyme, a protein that speeds up one chemical change. This one, phospholipase, works like scissors: it snips a fatty tail called arachidonic acid free from the membrane. Every signal that follows is built from it.
Build the idea
Freed arachidonic acid can take two roads. One runs through cyclooxygenase, called COX for short; the other runs through lipoxygenase. Both are enzymes, and each turns arachidonic acid into a different family of signals.
Build the idea
COX-1 is the everyday form of COX, at work in most tissues all the time. It makes prostaglandins, short-lived local signals. In the stomach they keep up the stomach shield, a slimy, acid-cancelling coat over the lining (Lesson 16).
Build the idea
Platelets are tiny cell pieces in the blood that clump together to plug a leak in a blood vessel (Lesson 12). Their COX-1 makes thromboxane, a signal that calls more platelets to stick and clump.
Build the idea
COX-2 is the second form of COX. Most tissues hold little of it, but injured cells quickly make much more. At the injury, COX-2 pours out the prostaglandins that drive inflammation.
Build the idea
These prostaglandins widen and loosen nearby blood vessels, so the area reddens and swells. They make pain nerves more sensitive. In the brain they turn up the body’s thermostat, causing fever: a raised body temperature. The new meter tracks pain, swelling and fever together.
Build the idea
Down the other road, lipoxygenase makes leukotrienes. They call in white blood cells, the body’s defence cells, and squeeze the airways, the breathing tubes of the lungs. Too much of them helps narrow the airways in asthma, a lung condition with wheezy breathing.
Build the idea
Injury frees arachidonic acid. COX-1 keeps up the stomach shield and platelet clumping; COX-2 drives pain, swelling and fever; lipoxygenase makes leukotrienes. Two key measures sum it up: how much pain, swelling and fever, and how strong the stomach shield is.
What changes it
Non-steroidal anti-inflammatory drugs (NSAIDs, not steroids), such as ibuprofen, plug both COX-1 and COX-2 for a while. Pain, swelling and fever fall, but the stomach shield thins and platelets clump less. A little arachidonic acid spills toward leukotrienes.
What changes it
COX-2 selective inhibitors, such as celecoxib, plug COX-2 but leave COX-1 working. Pain, swelling and fever fall; the stomach shield and platelet clumping stay near normal. Blood vessels and kidneys still need some COX-2 prostaglandins, so risks remain.
What changes it
Aspirin blocks COX for good by sticking a chemical tag onto it. Most cells can build new COX, but platelets cannot, so their thromboxane stays low and clumping stays down for the platelet’s whole life. Pain and swelling ease; the stomach shield thins.
What changes it
Glucocorticoids, steroid medicines copied from the body’s stress hormone cortisol (Lesson 15), such as prednisone, work higher up. They slow the phospholipase scissors and stop cells making extra COX-2, so prostaglandins and leukotrienes both fall.
What changes it
Leukotriene modifiers, such as montelukast, block leukotrienes where they act on the airways, or block lipoxygenase itself. The airway squeeze eases, which helps prevent asthma attacks. COX and its prostaglandins carry on untouched, so pain and swelling stay.
Start with Next, or use the arrow keys. Pictures are illustrative, not measurements.
Loading reference values…
Normal teaching baseline.
The blue line on each bar, and the large number beside it, show where an illustrative teaching model sits: not a patient measurement and not a sourced value. The shaded bands are the reference ranges quoted under each row; where a source gives only one typical value, a dark tick marks it instead. Selecting a drug or condition shows the expected direction of each value, compared with a normal body, and applies that state to the model. Where no direction is cited, no arrow is shown and the model holds that value where it was.
NSAIDs, COX-2 selective inhibitors and leukotriene modifiers are animated in the Lesson and in Explore freely, but they are not listed as states here: no open reference with a checked excerpt giving their direction on these values was available to this page, and every state on this tab must quote its source.
Blood pH and acidosis are taught in Lesson 11: Acid–Base Balance; glucocorticoids and blood glucose in Lesson 15: The HPA Axis and Steroids.
An illustrative teaching model of one injured patch of tissue, its platelets and the stomach lining. Change how badly the tissue is hurt, add drugs (they combine), and watch the flows and the four meters. Dashed marks are the untreated injury, this lesson’s normal; solid marks are your settings.
Everything is worked out relative to the untreated injury and settles at once; there is no time course. Phospholipase frees a trickle of arachidonic acid at rest and more as the injury grows. COX-1 is always present; COX-2 is made in proportion to the injury. At the injury COX-2 does most of the work, so the prostaglandins behind pain, swelling and fever follow COX-2 far more than COX-1. The stomach shield and platelet clumping follow COX-1 alone. Arachidonic acid that COX cannot take spills a little toward lipoxygenase, so blocking COX raises leukotrienes slightly.
An NSAID plugs a share of both COX enzymes; a COX-2 selective inhibitor plugs COX-2 only; aspirin tags COX-1 almost completely and COX-2 less so, and because platelets cannot make new COX its effect on them lasts. A glucocorticoid slows phospholipase, stops much of the extra COX-2 being made and damps inflammation in other ways too. A leukotriene modifier blocks leukotrienes where they act, so the airway squeeze falls while leukotrienes are still made. The sizes of every effect are illustrative; only their directions are meant to teach.
Left out: prostacyclin, the blood-vessel prostaglandin whose loss under COX-2 selective inhibitors is part of their heart risk; the kidney’s prostaglandins; other routes for arachidonic acid; the many other inflammatory signals; how drugs are absorbed and cleared; and every real-world difference between people. Nothing here is a prediction for a real person, and nothing here is a treatment plan.