Acute Inflammation | Immunology
Summary
TLDRThis lecture delves into acute inflammation, a rapid immune response to injury or infection. It outlines the nonspecific nature of inflammation, its purpose to neutralize irritants and initiate repair, and its various causes, including microbes and physical trauma. The lecture highlights the clinical features of inflammation, both local and systemic, and explains the two-phase process involving vascular and cellular responses. It concludes with the possible outcomes: complete resolution, replacement with fibrotic tissue, or progression to chronic inflammation.
Takeaways
- 🔍 Acute inflammation is a rapid, short-term response of the immune system to injury or infection.
- 🛡️ The primary purpose of acute inflammation is to neutralize the injurious agent, prevent its spread, and initiate the healing process.
- 🌡️ Causes of inflammation include microbes, physical trauma, radiation, temperature extremes, chemicals, ischemia, foreign substances, and immune system overreactions.
- 🏥 Clinical features of acute inflammation are categorized into local (redness, heat, swelling, pain, loss of function) and systemic (fever, increased heart rate, increased white blood cells, etc.).
- 🩺 The suffix '-itis' in medical terminology indicates inflammation of a specific body part, such as 'colitis' for colon inflammation.
- 🔬 The process of acute inflammation involves two main phases: the vascular phase (vasodilation and increased permeability) and the cellular phase (white blood cell activity).
- 🚨 Histamine, prostaglandins, and cytokines are key chemical mediators that initiate and sustain the inflammatory response.
- 🔄 Neutrophils play a crucial role in the early stages of acute inflammation by migrating to the site of injury, phagocytosing bacteria, and dead cells.
- 🔄 Macrophages become active in the later stages, aiding in the removal of debris and contributing to the resolution of inflammation.
- 🌟 Possible outcomes of acute inflammation include complete resolution, replacement with fibrotic tissue (fibrosis), or the development of chronic inflammation.
Q & A
What is acute inflammation?
-Acute inflammation is a rapid, nonspecific response of the innate immune system that occurs in vascular tissues and is characterized by a short time frame, coming on quickly and then resolving.
What is the purpose of acute inflammation?
-The purpose of acute inflammation is to neutralize the injurious agent, potentially remove or seal it off from the rest of the body, and initiate the wound healing process.
What are the common causes of acute inflammation?
-Common causes include microbes such as bacteria, viruses, and fungi; physical trauma; radiation; burns; chemicals; ischemia; foreign substances; and immune system overreactions like hypersensitivity disorders.
What are the local clinical features of acute inflammation?
-The local clinical features include redness, heat, swelling, pain, and loss of function, which are typically localized to the area of injury or infection.
What are the systemic clinical features of acute inflammation?
-Systemic clinical features include fever, an acute phase protein release from the liver, leukocytosis (increase in white blood cells), increased heart rate, increased blood pressure, increased respiratory rate, and symptoms like anorexia and malaise.
What does the term 'itis' indicate in medical terminology?
-In medical terminology, the suffix 'itis' indicates inflammation. For example, colitis is inflammation of the colon, appendicitis is inflammation of the appendix, and dermatitis is inflammation of the skin.
What are the two main phases of the inflammatory process?
-The two main phases of the inflammatory process are the vascular phase, involving vasodilation and increased vascular permeability, and the cellular phase, involving the migration of white blood cells to the site of injury.
How do neutrophils play a role in acute inflammation?
-Neutrophils are the most abundant white blood cells in acute inflammation. They become phagocytic, eating up damaged cells and bacteria, and are crucial for the removal of the injurious agent.
What are the three possible outcomes of acute inflammation?
-The three possible outcomes of acute inflammation are complete resolution, where the injurious agent is removed and the tissue is repaired; replacement, where damaged tissue is replaced by connective tissue like collagen, leading to fibrosis; and chronic inflammation, which occurs if the agent is not removed or if there is an ongoing immune response.
How does the body initiate the healing process during acute inflammation?
-The body initiates the healing process during acute inflammation by activating fibroblasts, which are connective tissue cells that lay down collagen to repair and seal off the area of injury.
Outlines
🔍 Introduction to Acute Inflammation
This paragraph introduces the topic of acute inflammation, outlining the lecture's six key points: definition, purpose, causes, clinical features (both local and systemic), the process (pathophysiology), and outcomes of inflammation. Acute inflammation is distinguished from chronic inflammation by its rapid onset and short duration. It is a nonspecific response of the innate immune system, which is always present and reacts uniformly to various injuries, regardless of their nature. The paragraph emphasizes the importance of understanding inflammation's role in the body's response to injury and the subsequent healing process.
🌡 Clinical Features of Inflammation
The second paragraph delves into the clinical features of inflammation, which are divided into local and systemic effects. Local effects are the classic signs of inflammation: redness, heat, swelling, pain, and loss of function. These are typically confined to the area of injury. Systemic effects, on the other hand, affect the entire body and can include fever, increased production of acute phase proteins by the liver, leukocytosis (increase in white blood cells), elevated heart and respiratory rates, and feelings of anorexia or malaise. The paragraph also touches on medical terminology, explaining that 'itis' suffixes indicate inflammation of a specific body part, such as colitis or appendicitis.
🩸 The Process of Inflammatory Response
Paragraph three explains the process of acute inflammation, which involves two main stages: vascular and cellular. The vascular phase includes vasodilation, leading to increased blood flow and the classic signs of redness and heat, and increased vascular permeability, causing fluid and cells to leak into the surrounding tissue, resulting in swelling. The cellular phase involves the migration of white blood cells, particularly neutrophils, to the site of injury. These cells are crucial for phagocytosing damaged cells and pathogens, thus playing a key role in the resolution of inflammation. The paragraph also discusses the release of chemical mediators like histamine, prostaglandins, and cytokines, which are instrumental in initiating and sustaining the inflammatory response.
🧬 Cellular Phase and Systemic Effects
This paragraph continues the discussion on the cellular phase of inflammation, focusing on the role of neutrophils and macrophages. Neutrophils are the first responders, arriving at the site of injury within 24 to 48 hours, and are responsible for phagocytosing bacteria and damaged tissue. Macrophages arrive later, peak after 48 hours, and are involved in the cleanup and resolution phase. The paragraph also details the systemic effects of inflammation, such as fever, increased heart rate, respiratory rate, and blood pressure, which are mediated by cytokines like interleukin 1 and tumor necrosis factor-alpha. These systemic responses are part of the body's overall reaction to inflammation and are crucial for the immune system's efficiency.
🏁 Outcomes of Acute Inflammation
The final paragraph wraps up the lecture by discussing the possible outcomes of acute inflammation. These include complete resolution, where the cause of inflammation is removed, and the tissue is repaired; replacement with fibrosis, which occurs when the damaged tissue, such as heart muscle after a heart attack, is replaced by connective tissue, leading to potential organ dysfunction; and chronic inflammation, which can result from unresolved inflammation or ongoing immune responses, such as in autoimmune diseases. The paragraph emphasizes the importance of understanding these outcomes to appreciate the body's complex response to injury and the potential consequences of inflammation.
Mindmap
Keywords
💡Inflammation
💡Innate Immune System
💡Vascular Tissue
💡Vasodilation
💡Chemical Mediators
💡Endothelial Cells
💡Exudate
💡Neutrophils
💡Macrophages
💡Systemic Effects
💡Resolution
Highlights
Inflammation is a rapid, nonspecific response of the innate immune system to injury or infection.
Acute inflammation is distinguished from chronic inflammation by its short time frame and swift resolution.
The purpose of inflammation includes neutralizing the injurious agent, sealing off the affected area, and initiating the repair process.
Causes of inflammation range from microbes and physical trauma to chemicals, ischemia, and immune system overreactions.
Clinical features of inflammation are categorized into local, such as redness, heat, swelling, pain, and loss of function, and systemic, like fever and increased heart rate.
The suffix '-itis' in medical terminology indicates inflammation of a specific body part, such as colitis or appendicitis.
The process of acute inflammation involves two main phases: vascular, characterized by vasodilation and increased permeability, and cellular, involving white blood cells.
Histamine, prostaglandins, and cytokines are key chemical mediators that initiate the vascular phase of inflammation.
Vasodilation leads to increased blood flow, resulting in redness and heat, which are early signs of local inflammation.
Increased vascular permeability allows plasma, proteins, and cells to leak into the tissue, causing swelling.
Pain and loss of function are clinical signs resulting from sensitization of nerves and pressure due to swelling.
Neutrophils play a crucial role in the cellular phase by migrating to the site of injury and phagocytosing bacteria and dead cells.
Macrophages arrive later in the inflammation process, aiding in the clearance of debris and contributing to resolution.
Systemic effects of inflammation include fever, leukocytosis, and changes in heart rate, blood pressure, and respiratory rate.
Cytokines like TNF-alpha and interleukin 1 are responsible for systemic responses to inflammation.
The outcomes of acute inflammation can be complete resolution, replacement with fibrotic tissue, or progression to chronic inflammation.
Fibroblasts are essential for tissue repair by laying down collagen, which can lead to fibrosis if muscle cells are extensively damaged.
Chronic inflammation involves different cells, such as monocytes and lymphocytes, and can result from ongoing immune responses or unresolved agents.
Transcripts
welcome to this short lecture on acute
inflammation in this lecture we'll cover
what is inflammation what's the purpose
information what causes inflammation
what are the clinical features of
inflammation what's the process of
inflammation and finally what's the
outcome of inflammation so for this
video on acute inflammation we're going
to essentially cover these six points
what is it what's its purpose
what's its cause the clinical features
both locally and systemic Lee the
process which is essentially the
pathophysiology and then finally what
are the outcomes so starting off with
what it is so inflammation or acute
inflammation the name acute suggests
that's probably got a short time frame
so it comes on rapidly and then it
disappears not to be confused with
chronic inflammation which we'll cover
at another date
so the inflammation itself is a
nonspecific part of the immune system so
with the immune system we have the
innate and the adaptive so we're
focusing on the innate so it's always
there and it will react always the same
regardless of what's causing the injury
so like the anatomy part of your innate
immune system which is like your skin or
your mucous membranes or your tears or
your wax the inflammation is a
physiological reaction of the innate
immune system so it is a process it
reacts regardless if it's a bacteria
it's regardless if it's a an ischemic
injury or a physical injury it will just
happen the same way it has to happen in
vascular tissue so will only occur
within vascular parts of your body parts
of your body that have a blood supply
and it's important to note that it's
nonspecific so always will happen the
same way what's the purpose of it so
this is the second point well it will
neutralize the in Juris agent so
whatever's causing the inflammation it
will neutralize it hope
remove it it may seal it up from the
rest of the body so if this was in your
hand
and it was from an infectious particle
it will seal it off and stop it
spreading elsewhere to the body so
that's a good thing to do and then
finally it helps with the repair so it's
very important it's starting off the
wound healing process the causes well
the causes are quite varied there's a
quite a long list a common one is
microbes so these are infectious
organisms that come into your body
invade your body and they will cause
damage to your body so it's important
that we have a inflammatory response to
this so this could be bacteria viruses
fungi the reactions the same so these
infectious particles will come in they
will have antigens with with or on them
and that will cause a process or the
inflammation process to start physical
trauma can cause inflammation such as
trauma like a being hit or punched or
something like that
radiation so like UV light can cause
inflammation burn so temperature whether
they're too hot or too cold will be a
cause of inflammation chemicals so this
would be like pH acids or bases can
cause inflammation ischemia so it's a
good example that's a good one so this
is a reduction in blood flow and then
therefore a reduction in oxygen so for
instance a myocardial infarction or a
heart attack that will cause
inflammation to the heart foreign
substances so this could be things like
let's say a splinter you get a piece of
wood that gets stuck in your skin or in
your wound that will continue to cause
inflammation because there are things on
it that your body's reacting to or maybe
if there's like suturing from a closure
of a wound there could be certain
material in that suture that would cause
reactions and ongoing reactions
thus inflammation and then finally your
immune system so sometime
your immune system over reacts and this
is what we call hypersensitive disorders
or reactions so a good example of that
is the type 1 hypersensitivity disorders
like you react to pollen or peanuts
these aren't really damaging substances
but for some reason for some individuals
you their immune system over reacts
releases too much histamine and then
that causes the inflammation so there
are some examples of causes
that will cause inflammation to occur
moving on to clinical features this one
is really important and not only is it
important to know what these features
are but when we go through the process
itself it's good to know the mechanisms
that leads to it so the clinical
features are categorized into two you
have your local and you have your
systemic the local are the classic
features that you hear about when you
study inflammation being the classical
four signs of inflammation sometimes
then they're in Latin so sometimes
they're called rube or Cal or two Mar
del or if it's not Latin it would be
redness heat swelling pain and then the
fifth one is loss of function so this is
usually always localized so if it was in
your hand you had any inflammation you
would have redness heat swelling pain
loss of function in your hand whereas
the systemic effects this is whole body
so some good examples and these are the
ones you should know fever you have an
acute protein plate and protein release
from the liver leukocytosis so an
increase in white blood cells in your
blood your heart rate will go up your
blood pressure will go up your
respiratory rate will go up and even
things like anorexia which is lack of
wanting to eat or maybe malaise you just
feel rundown or just tied lethargic so
there the clinical features we'll go
through and explain what causes those
before we jump into the process it's
also important to note within the
medical terminology you would hear the
soft suffix chord itis
itis means inflammation what so whenever
you hear a body structure with itis it
refers to that structure being inflamed
such as if you have a inflammation of
your colon colitis if you have
information of your appendix
appendicitis if you have an
upper-respiratory fact tract infection
that would be bronchitis or laryngitis
if you have inflammation of your joints
that would be arthritis if you have
inflammation of your skin that would be
dermatitis so that's important to know
when you're looking at the medical
terminology itís always means
inflammation so let's go now to the
process this is the crux of this lecture
how does it happen what causes it to do
this so the before we get into this
image the first thing you need to be
aware of with acute inflammation there's
a two stages or two main steps there is
the vascular which refers to the blood
vessel and then there's cellular which
refers to the cells usually inflammation
we'll go into three steps they're the
two categories but the three steps been
vasodilation so blood vessel gets bigger
permeability becomes more leaky and then
cellular or white blood cells go in and
remove the injury or the cause so let's
go through the process now before we
before we start just so you know what
this image is this top layer is your
epidermis this is the hypodermis or
dermis and this is your blood vessels so
this is where we're going to do our
particular implement inflammatory
process today so I'll get rid of the
tight title and what I'm gonna do is I'm
gonna cause an injury to the skin so
let's say you stood on a thorn
so the thorn came through and punctured
your skin so the cause in this case
could be probably two things coming off
the thorn would
a whole lot of bacteria so there would
be microbes this would cause the start
of the inflammation but there will also
be the trauma of all the cells here so
we would get a lot of necrotic tissue so
it's important to note with the causes
like the physical cause of the chemical
cause the ischemic cause these will
cause tissue death or necrosis and it's
the necrosis or the dead cells like here
that would start the process of so let's
just say we have dead cells with
bacteria now sitting within these under
under the skin we would have a whole lot
of resident cells so we might have mast
mast cells we might have some
macrophages up here we might have some
dendritic cells okay so there's a whole
lot of cells that are sitting around
which are part of the immune system
waiting for something to happen plus all
the cells that have been injured now
what happens with these cells the
Marcelle is a good one it releases a
chemical which we call histamine
macrophages is another good one so these
are big sellers they would release
something called prostaglandin and
there's other cells in here which might
just release cytokines
so the first part of the inflammatory
process to be aware of is you need to
have some kind of caused some kind of
injurious agent and then we need to
produce pro-inflammatory chemical
mediators in this case histamine
prostaglandins cytokines now these
chemicals will go to the blood vessel so
this is the first phase this is the
vascular phase what the blood vessel
will do predominantly with histamine so
histamine will go here the blood vessel
will dilate
the walls or the sphincter will get
bigger that will cause more blood flow
to the region
so vasodilation is the first step this
is caused by the chemical mediators
pratik particularly the histamines so
blood vessels dilate get bigger more
blood comes to the region so this as
you'd imagine if you bring in more blood
flow to the area that's going to be your
first two localized
clinical signs being redness and heat
more blood it's going to go red more
blood it's going to bring temperature
hot okay so that's the first step as it
brings more blood okay there's going to
be more flow which is good because it's
going to bring white blood cells to help
with the removing all this problem okay
the next step that happens with these
chemical mediators what they're going to
do is also go to these cells here that
line your blood vessel these are called
endothelial cells okay now they are
usually stuck together holding hands
okay but with the chemicals the
cytokines the histamines that will cause
them to retract so these cells will
actually get smaller okay so as they get
smaller what that will do okay is start
to put holes in the blood vessels well
it's not really holes but just gaps and
so what that would do it would cause
more fluid to go out now the fluid that
comes out is plasma so that's the watery
portion of your blood but it also will
have cells in it and it will also have
plasma proteins in it so as that goes in
that's going to cause a process called
exudate exudate is a term that means
plasma fluid and proteins and cells
opposed to transudate which just means
plasma so this has got things in it so
plasma
proteins which is important like
complement proteins which would
hopefully try to kill off that bacteria
but also kinase which also helps with
the resolution of that injury so fluids
going to rush out as this process this
process of endothelial retraction is
what we call vascular permeability so
it's an increase vascular permeability
this is the second part of the vascular
phase so the first part was vasodilation
increase in blood vessel diameter more
blood flow comes to the area the second
phase of the vascular phase is
endothelial retraction which means the
cells get smaller and that means more
fluid leaves and we get extra date as
you'd imagine as you get extra date you
get swelling so there's the tissue
swells up this is the third localized
sign being swelling so the extra date is
now activated or now occurring now with
some of the plasma proteins they're
going to be activated like the kinds so
the Cullens
particularly ready cunning it's a good
one okay and what that's important for
is census sensitizing your nerves so
let's just say in your skin here you had
nerves okay now with the combination of
bradykinin also prostaglandin and also
all that swelling is going to cause
these nerves to be ultra sensitive very
very sensitive and as these
sensitization of these nerves increase
from a combination of Braddock Kenan
prostaglandins and just pushing on it
from the light swelling it's going to go
back to your brain and say this is
painful so this is the fourth sign of
inflammation being pain probably the
combination of the extra date and the
pain is going to lead to the fifth sign
being the loss of function so there you
go that's the five localized science I
of inflammation there now we move into
the third phase which is the cellular
phase
so as this vascular phase is that
happening and we losing all the fluid
out into the tissue what happens to the
composition of the blood in here is it
actually becomes more viscous thicker
because you've lost all the fluid now
what happens is all the red blood cells
accumulate in the middle because they're
smaller so there's a column of blood
flow in the middle being all your red
blood cells okay now the bigger the
bigger white blood cells come off to the
side so like the big neutrophils come to
the side now neutrophils are the most
abundant white blood cell and they're
the most important white blood cell for
acute inflammation so they're getting
pushed off to the periphery because the
blood flow is slow now all the red blood
cells sit in the middle and the white
blood cells in this case the neutrophil
sits up at the side so this is what we
call margination so they get pushed off
to the endothelial cells and they slowly
roll down the outside of the blood
vessel now with the cytokines cytokines
histamines etc they're going to the
endothelial cells which will make them
more adherent and that means the
neutrophils get stuck on them and then
they'll actually start popping out so
the neutrophils will actually squeeze
through and start coming out into the
tissue now they will follow through a
chemical gradient called chemotaxis
they will follow where the injury is
this could be a combination of chemicals
from the dead cells antigens from the
bacteria or the the chemicals released
from these cells like the macrophages
the mast cells the dendritic cells like
cytokines so they're actually going to
follow it and go to that area
neutrophils are important because they
are
start eating up all the damaged cells
and all the bacteria so they become
actually phagocytic so they start
chewing up and eating up now neutrophils
okay
neutrophils are very short lasting so
they will generally come on the scene
between 24 to 48 hours that's their peak
time on inflammation whereas later on
macrophages will come after 48 hours or
that's when they will peak macrophages
will come from monocytes monocytes or
white blood cells this process takes
longer
whereas neutrophils the upregulation
within the white blood cells or the
creation of new white blood cells in the
bone marrow happens very quickly
macrophages takes longer and that's why
it peaks at a later date so the
neutrophils come in they go through they
go to the area they start eating up dead
tissue and bacteria and this is probably
we're going to get a lot of the pus come
in because there's a whole lot of dead
cells and bacteria and so forth now at
the same time we've got all those
cytokines such as I'll pull out here
interleukin 1 T and F alpha so that
would be chiba necrosis factor-alpha
these are released by these cells and
these camp cytokines go into the blood
and that will then go systemically so
these tnf-alpha and interleukin 1
actually then goes and the blooding goes
everywhere so these these ones here are
now examples of what's causing systemic
effects so these chemicals will go up to
the brain and cause your hypothalamus to
change its set point so it's instead of
setting at 37 degrees Celsius it's going
to go up to 39 degrees and that's going
to cause you to have a fever
so that's a systemic response it's also
going to go to your bone marrow and tell
you to make more white blood cells so
this is the leukocytosis also remember
that your white blood cell
work better in a hotter temperature so
when this fever goes up your white blood
cells are probably going to do a better
job in a more efficient job as the
temperature is higher these cytokines
also go to your liver and produce more
plasma proteins like the complement
proteins like the coining 's okay it's
also going to go to your brain and tell
you to that you're starting to feel a
bit maybe nauseous but also anorexic so
you're not going to eat feeling
lethargic now as a result of the fever
your body needs to bump up its metabolic
rate so your heart rate will go up your
breathing will go up your blood pressure
will go up and this is the reaction the
systemic reaction to the inflammation so
what you see now is the process itself
has two main phases the vascular phase
the cellular phase the cellular phase is
a combination of the cells that started
the release off but then these white
cells take over to hopefully remove the
agent and neutralize with the extra date
and hopefully cause whatever caused the
problem to be removed away so this leads
to the outcome the outcome of acute
inflammation is three there's either a
complete resolution which means the
aging gets taken away this gets
neutralized and removed and the skin
gets closed up another thing that I
forgot to mention is also these
chemicals are good and important for
activating fibroblasts so these are
connective tissue cells which will come
into the area and start to repair it so
that will if you remove this thorn the
photo blast will start to lay down
collagen and hopefully seal that off and
then you repair so that would be
resolution if you remove the agent and
it gets completed then you'll have
complete resolution now if it wasn't
perfect
if particularly you cause damage to
parts of the body that can't
pair itself like the heart so if that
wasn't a skin but that was your heart
and you had a heart attack muscles of
your heart can't replace themselves so
what happens is the fibroblast lay down
over where the muscle cells died and you
replace muscles with collagen which
means that now you have a fibrotic
reaction or fibrosis now that could be
okay if it's a small degree of injury
but if it's a big part of your heart
that's died you're going to lose a lot
of muscle and then have connective
tissue which would result in a negative
outcome and maybe the patient will die
or have a degree of heart failure
because it can't pump effectively
anymore that could be also a problem in
the lungs if you have things like
pneumonia or in the liver if you were to
have inflammation and you then had scar
tissue and that would lead to something
like cirrhosis finally the third outcome
that could take place would be chronic
inflammation so if you don't remove the
agent or if it's a really serious
infection like a viral infection or if
you have an ongoing immune response like
an autoimmune disease you will have
chronic inflammation so this is an
ongoing inflammatory process there are
different cells that are involved in
chronic inflammation such as monocytes
and lymphocytes but this is a
long-standing
impliment inflammation unlike this one
which is acute and it will disappear
after a few days so there you have it
that's acute inflammation hopefully it
all made sense so hopefully now you know
what is inflammation what's the purpose
of inflammation what's the cause of
information you know the clinical
features and you know what causes the
clinical features you know the process
the two main steps vascular and cellular
and then you know the three possible
outcomes been resolution replacement or
chronic inflammation
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