In this section of basic pathology we will take a look at
inflammation and wound repair. Organization will be
acute inflammatory mediators quickly reviewing that what you
have seen in Immunology. Going into chronic inflammation,
and a few words about wound repair. To begin with, take a
look at the various cells that are involved in inflammation.
When we talk about WBC's, you should be able to identify many of
this cells. Remember in acute inflammation, it's a fact that
neutrophil are coming in. And neutrophils as you see in the
picture are properly segmented. Not hypersegmented but
definitely segmented. Approximately 4 to 6 lobes is what you are
expecting to see. At some point in time, if chronic inflammation
is what's occuring, then it is the monocyte that is being
recruited. And you notice here that the nucleus of a monocyte
should be approximately the size of an RBC and you notice that
the monocyte and it's nucleus should be quite circular.
Versus for example; When you deal with infection such as viral. That
will be CMV or EBV. There is every possibility that now,
this monocyte then becomes what's known as an atypical monocyte.
Monocyte will be in circulation. If a monocyte then ends up
in your tissue you then call this a macrophage. In acute
inflammation, the cardinal signs that you would expect to see
would be rubor, redness; calor, heat; tumor, swelling; pause here
for one second. The reason I say that is I will quickly walk
you through acute inflammation and the different changes. And you
have seen this before, in immuno. For example, let's say
that there is an antigen, a bacteria that is now been introduced
into the interstitium. What has to happen is that the neutrophil,
which is the acute inflammatory cell has to move from your
circulating pool over to the marginating pool.
We'll talk about quickly once again, review some of those mediators
including your selectins, pherolins, integrins for proper adhesion.
And then finally getting through your endothelial cell. A process
known as diapedesis. Now the diapedesis or transmigration
would then get the neutrophil out in interstitium but in order
for your neutrophil to get out into the interstitium,
what does the blood vessel has to do? Not vasoconstrict but
vasodilate. When you vasodilate, the mediator here please.
Do you remember? That's responsible for the eventual or should I
say very quick vasodilation. Would be histamine. If you
vasodilate are'nt you creating a inflammatory state? Sure. The
swelling, the tumor. If you increase in amount of blood flow
to that area, then you would expect to be increased redness. So,
rubor. With increase blood flow to this area,
you would also expect there to be emission of heat. Calor, think
of burning calories. At this point, 3 of the 5 cardinal signs
of acute inflammation; rubor, calor, tumor, is then being
created by histamine on purpose. And the reason for this
is because of neutrophil has to then get through the gap
junction of the endothelial cell into the interstitium.
And there you will have, and we will talk about a few
chemotactic factors and those opsonins. Dolor, pain.
Histamine will be the major mediator and bradykinin responsible
for pain. The picture, if it's a bacterial infection,
erysipelas, meaning to say that here due to that acute
inflammatory response there is quite a bit of reddening
that you can expect because of acute inflammation. The key cells
of acute inflammation will be neutrophils. And here the dark
cells that you see in this particular structure would then indicate
recruitment of your neutrophils in great number. If you were to then
blow up a neutrophil then you would expect to see what kind of
cell? A segmented neutrophil. Remember in certain issues
such as B-12 deficiency or folate deficiency in which you may then
result in hypersegmented type of neutrophil which is a primitive cell.
In the very beginning of this I actually showed you a band cell.
What does a band cell mean to you? It's a very primitive neutrophil.
And there should be a certain number of Band cell in circulation
but if there is acute inflammation, you can imagine now
that the band cell number would be increased. Do not forget that
if you are dealing with neutrophils, or in general,
if you are dealing with a tri-lineage of cells of your hematopoietic
or your stem cells that you should be beginning from the bone
marrow always. Remember neutrophil will be the most abundant type
of a granulocyte or a WBC followed by eosinophils and basophils.