Acute Inflammation | Immunology

Summary

This 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

00:00

🔍 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.

05:02

🌡 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.

10:02

🩸 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.

15:04

🧬 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.

20:05

🏁 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.

Keywords

💡Inflammation

Inflammation is a protective response from the body's immune system to harmful stimuli, such as pathogens, damaged cells, or irritants. In the context of the video, acute inflammation is emphasized, which is a rapid and short-lived response to injury. The video explains that inflammation is a nonspecific reaction, meaning it occurs in a standard way regardless of the cause of the injury, and it is part of the innate immune system, which is always present and reacts similarly to various threats.

💡Innate Immune System

The innate immune system is the body's first line of defense against infections and other harmful stimuli. It is nonspecific and acts immediately, in contrast to the adaptive immune system, which is more specialized and takes time to respond. The video underscores the role of the innate immune system in acute inflammation, highlighting its role in the initial response to injury or infection.

💡Vascular Tissue

Vascular tissue refers to the parts of the body that are supplied with blood vessels, allowing for the transport of blood, oxygen, and nutrients. Inflammation, as discussed in the video, occurs within vascular tissue, emphasizing the importance of blood supply in the inflammatory response. The video explains that the process of inflammation involves changes in blood vessels, such as vasodilation and increased permeability, which facilitate the delivery of immune cells and other components to the site of injury.

💡Vasodilation

Vasodilation is the widening of blood vessels, which increases blood flow to a particular area. In the video, vasodilation is described as the first step in the vascular phase of inflammation. It is caused by chemical mediators like histamine, leading to redness and heat at the site of injury, which are part of the classical signs of inflammation.

💡Chemical Mediators

Chemical mediators are substances that are released during an immune response and help to regulate the inflammatory process. Examples mentioned in the video include histamine, prostaglandins, and cytokines. These mediators are crucial in the development of inflammation as they cause vasodilation, increased vascular permeability, and attract immune cells to the site of injury.

💡Endothelial Cells

Endothelial cells line the interior surface of blood vessels and lymphatic vessels. The video describes how, during inflammation, chemical mediators cause these cells to retract, increasing the vascular permeability and allowing fluid, proteins, and cells to leak out into the surrounding tissue, contributing to swelling and the formation of exudate.

💡Exudate

Exudate refers to the fluid that leaks out of blood vessels during inflammation. It contains plasma, proteins, and cells, which help in the immune response. The video explains that exudate is a result of increased vascular permeability and is part of the body's attempt to deliver immune cells and proteins to the site of injury to combat infection or repair tissue.

💡Neutrophils

Neutrophils are a type of white blood cell that plays a critical role in the immune response, particularly in acute inflammation. The video describes how neutrophils are attracted to the site of injury by chemical gradients and become phagocytic, engulfing and destroying pathogens and damaged cells. They are among the first responders in the cellular phase of inflammation, peaking within 24 to 48 hours after the onset of inflammation.

💡Macrophages

Macrophages are large immune cells that originate from monocytes and are crucial in the later stages of inflammation. The video mentions that macrophages peak after 48 hours and are involved in the removal of dead cells, pathogens, and the initiation of tissue repair. They also play a role in chronic inflammation if the inflammatory stimulus persists.

💡Systemic Effects

Systemic effects refer to the body-wide responses that occur during inflammation. The video explains that systemic effects include fever, increased heart rate, increased white blood cell count (leukocytosis), and feelings of malaise or anorexia. These effects are due to the action of cytokines and other chemical mediators that circulate in the blood, affecting the entire body and not just the localized site of inflammation.

💡Resolution

Resolution in the context of inflammation refers to the successful removal of the cause of inflammation and the subsequent repair of the affected tissue. The video describes how complete resolution involves the neutralization of the injurious agent, the repair of tissue by fibroblasts, and the return of normal tissue function. It contrasts with other outcomes such as fibrosis or chronic inflammation, where the inflammatory process does not fully resolve.

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