okay great so my topic will be inflammation oh wait i'm just fixing things wait Okay, so my topic is about inflammation and repair. So in definition, inflammation is a response of vascularized tissue to infection. Actually it's not just infection, any cellular injury, any damage to the tissue or to the cell, so it brings cells and molecules of the host defense.
from the circulation to the sites that are needed in order to eliminate the offending agent. So it's a mechanism. For example, you have a t-shirt, so all of that, whatever the cause is, it will cause inflammation. So there are two features of inflammation. It can either be acute.
and chronic inflammation. When you say acute inflammation, it is usually fast. So it occurs abruptly. So kung ngayon natalisod ka or nabubog ka, lalabas ngayon ang acute inflammation.
When you say chronic, it's either from acute inflammation and hindi na-resolve, going to chronic, or it can also be because the severity of the injury is... it's very big that it can lead to chronic inflammation okay so onset of acute inflammation it is fast it can occur in minutes or hours while in chronic so it's low so it it um it can occur after a few days a few weeks or a few months so the feature of sinabing acute inflammation makikita niyo sa microscope they are mainly neutrophils um while in chronic inflammation you will see abundance of monocytes or macrophages and also lymphocytes. For tissue injury and fibrosis, meaning the effect in acute inflammation, they are usually mild and self-limited, while in chronic, they are often severe and progressive.
And local systemic signs and symptoms are very prominent in acute inflammation. So for example, Can you hear me? Can someone answer me? Yes.
Okay. So for example, meron kang kaklase, inubuhan ka. So after, in acute inflammation, usually systemically or locally, pwede kang magkalagnat. So those are acute inflammation.
In injuries naman, may kita niyo, mamumula na siya kagad. So, ganun yung acute inflammation. So, there are five cardinal signs of inflammation. So, ano to? So, pag nakinam mo tong limang to, most probably, there are inflammations.
So, kung mag-iinit, pag hinawakan, mapula. Can I speak Tagalog or there are foreign students? Okay, nobody's answering. Maybe I can explain in Tagalog.
So redness, namumula, swelling or tumor, ibig sabihin namamaga. Pain, syempre pag namamaga, mainit, the patient might experience pain and also loss of function. So what are the physiological rationales of this cardinal science? So when you say rubor or redness, please remember this table.
The redness in an inflamed area is usually caused by increased blood flow. When you say swelling, and also pala, the physiological rationale that I will go into explain now is usually part of an inflammatory process, okay? So, pag sinabing increased blood flow, ah, ano una niyo makikita, makakaroon ng redness.
Pag sinabing swelling or tumor, it is secondary to an increased exudation of fluid to the site of inflammation. Chlor or heat, it is due to increased blood flow, exudation of fluid, and also release of inflammatory mediators. When you say pain or dolor, it is caused by stretching of pain receptors and nerves by... inflammatory exudates so the band of maga so no mania rena caro no stretching non nerves non pain receptors and also it can be secondary to the release of chemical mediators during inflammatory process and the last one is functionally Lisa bucket no one will and function or loss of function because a mass a hit so no no no no no no no no no no no no no no no no no no no no no no no no And also, it can be due to disruption of tissue structure, and it could also be brought up about fibroplasia, which is a response to injury, or also metaplasia.
So what are the causes of inflammation? So this is not just an infection. This is not just a bacterial infection, viral, fungal, or parasitic infection. foreign body, tissue necrosis, and also an immune reaction. When you say infection, you can say viral, bacterial, fungal, and parasitic.
And the range of this type of inflammation, it can usually be from no damage at all to can be fatal. So for example, you got a viral infection, you just need to be careful, you just need to be careful. pero pwede it can progress to vitality. Next is foreign body. So, these are traumatic tissue injury.
And also, it can be endogenous and exogenous. Meaning, endogenous, pwede sa sariling katawan nang gagaling. Or these are endogenous substances that are deposited in the tissue that can cause an inflammatory reaction.
Okay? Next is tissue necrosis. Ano ba yung cost ng tissue necrosis? You should eat...
because of decreased blood flow such as in myocardial infarction and also because of ischemia. If the blood supply is lost in an area of the body, it can lead to tissue necrosis. And also tissue necrosis can be brought about by trauma, physical and also chemical injury, and also thermal injury.
Inflammation could also be caused by an immune an immune reaction. What do you mean by immune reaction? So it can be an autoimmune diseases, so which is an injurious response of the body against the self.
So pwedeng mga rheumatic heart disease for example, nagkaroon ng sugat ang bata and then meron mga strains toh that could affect the self-antigen. So ano nangyayari? ang naapektuhan will be the heart valves, sa nakakaroon ng sakit sa puso. Pero nagsimula lang siya sa sugat.
Another one are substances that are seen in the environment. So these are what we call allergens. So these are immune reactions that can also activate an inflammatory response.
Naintindihan? Or do I speak fast? Kaya pa?
guys can and anyone answer me yes okay so what are now the steps of inflammation so inflammation in any mechanism in any body mechanism uh everything will start with recognition so dapat ma-recognize ng katawan na ah wait meron akong injury okay so um so kailangan ma-recognize para magkaroon ng activation so next na recognize na nya okay uh nagkaroon ka ng sugat for example so na recognize ng katawan oh okay meron tayong sugat so anong gagawin they will now recruit uh leukocytes and also plasma proteins so what are these leukocytes so this are the this are cells uh used to uh they are host defense okay so soldiers bodies and also plasma proteins. So, pag nagkaroon na ng activation, nag-recruitment na, then nagkakaroon ng removal of agent. So, it can either be phagocytosis, autophagy, so yung mga ganon responses.
And then in any response, in any mechanism, dapat may regulation kasi I suddenly logged out. Hi, please somebody answer me. I have a septic inflammation. Okay, wait.
I'll go back. I don't know what happened but yeah, sorry. Can you see now? Okay. Yes.
Wait, wait, wait, wait. I'll check my Wi-Fi. Okay. okay going back so now do not I also removal of engine so but the top of the matina for example bacteria so the patina long inflammatory process and on the but my area next is to regulate the response to regulate inflammation or to stop an inflammatory process bucket because it by the Macaroni over response so it can cause injury also so kailangan ihinto nila okay next after matanggal na ma-regulate ang response then we'll go to repair okay so are different there are different mediators of inflammation so it can either activate trigger enhance the process or each process so it can either be cell derived or plasma protein derived so later on i will discuss this mediators now i'll go to acute inflammation so on the top fast occurring it occurs in minutes they usually present systemically and um and usually mild so there are three major components of inflammation so pag nagkaroon ng injury.
So, first is vasodilatation of the small blood vessel. Next is increased permeability of the microvasculature. And last one is the emigration of leukocyte.
So, unang-unang mangyayari is ano, magdadilate. Lalaki yung lume ng mga blood vessel. Bakit? Para makomodate yung pag travel of leukocytes and plasma proteins to the site of injury.
Next one is increased permeability. So from the blood vessel, these leukocytes will be released to the blood vessel. So this is the permeable blood vessel wall. And then last one is the emigration of leukocytes.
So before we go to the process, what will be the first thing accumulation so this our blood uh the first reaction is accumulation of uh fluid so it can either be an exudates so when you say exudates they are extravascular fluid that are rich in protein cellular debris and this is uh usually uh implies increased vascular permeability so it may not be so when you say nana or purulent exudates they are inflammatory exudates that are rich in leukocytes so you manganana rich in leukocytes and they're looking at the these are your neutrophils your macrophages or your monocytes and when you say um edema so it can be um secondary to accumulation of transudates when you say transudates these are uh ultra filtrate of blast blood plasma because of an imbalance in the um even without increased vascular permeability imbalance in hydrostatic pressure and oncotic pressure kakarana edema, nagkakarana transudates. So pag merong na na, ito yung mga tinatawag na exudates. Pag transudates, more on fluid, more on water, ang nagkakarana accumulation. Again, the difference between exudates and transudates, when you say transudates, these are due to imbalance in the osmotic and on hydrostatic pressure.
Usually, the fluid that accumulates in transudates they are low in protein and they have low specific gravity while it exudates because it is secondary to an increase in permeability so our vascular permeability so my ketone they are rich in protein and bucket because you will see accumulation of leukocytes yeah they've been transudi and neutrophils different types of of leukocytes and also cellular debris, yung mga nasira nila or yung mga effects or product ng inflammatory reactions. So what causes transudates? Usually, they are, sabi ko nga, imbalance in oncotic and hydrostatic pressure.
Ito din yung nakikita nyo pag meron na kakaroon ng congestive heart failure. So, nagkakaroon na accumulation of water sa lungs. So, ito yung mga transudates na nakikita.
Pero minsan, when you say exudates naman, when we talk about the lungs, ito naman yung mga nag-accumulate na mga plema. Pero pag tinignan nyo, iba rin ang consistency niya physically. So, high protein, cellular debris, medyo yellowish siya. Okay? Next changes or reaction is changes in the vascular flow and also the caliber.
The first thing that happens is vascular dilatation. So that is the earliest manifestation in acute inflammation. Remember, the earliest manifestation in acute inflammation is vasodilatation.
It comes together with stasis. So there is congestion. So it stays.
Because the blood vessel is enlarged, there will be accumulation, stasis, and congestion. At the same time, why is it congested? Because it causes a slow in the blood flow of the fluid in the blood vessel.
And in this condition also, it causes the leukocytes to... accumulates along the endothelium. So later on, I will discuss a different process in the emigration of leukocytes.
And this condition or this process or this step is mediated by histamine. So the next one, as I said earlier, vasodilatation, next is increased vascular permeability. So it means, these leukocytes Una na hindi siya kaya lumaban sa blood vessel, pero what happens in acute inflammation, kaya na nila mag-penetrate along the endothelium, along the blood vessel wall.
So this process or this step is the hallmark of acute inflammation. Okay, tandaan. Vasodilatation is the first event that happens in acute inflammation while increased vascular permeability is the hallmark of acute inflammation. Okay.
So it causes retraction of the endothelial cells along the blood vessel wall. So it can either be an immediate transient or it can be a delayed prolonged response. So when you say immediate transient, meaning it occurs rapidly.
So it occurs rapidly after exposure. But it might occur rapidly, but they are short-lived. So it can only appear.
or happens in 15 to 30 minutes. When you say delayed or prolonged, they are secondary to mild injuries such as burn injury, UV radiation injury, and this will lead to vascular leakage that occurs in a prolonged period of time. So they are delayed and prolonged. So it can occur after two hours and it can last after 12 hours.
So delayed prolonged meaning it lasts from 2 to 12 hours. So this delayed reaction is usually caused by contraction of endothelial cells or can be secondary to a mild endothelial damage. The next one, the next event is endothelial injury. So endothelial injury, it can cause necrosis and also detachment. And it is secondary to severe injuries.
Next is transcytosis. So transcytosis, this is an increased transport of fluid and also protein. And there's stimulation in this condition.
The. there is stimulation of intracellular channels that promotes uh leakages so all of this mechanism there is a big role of the lymphatic or lymphatic vessel or the lymphatic system so uh lymph flow um they help to drain the edema fluid that accumulates because of the increased vascular permeability um they could also drain leukocytes the cellular debris and also the microbes that causes the injury so ibig sabian parasan tung lymphatics na to so yung lahat nagiging product ng inflammation so ah dito na pupunta so yung mga nanana na accumulate natin because of an inflammatory process dumadaan sa sa limbs okay so don't you dumadaan sa live flow But if you are not careful, you will observe that there are some cells in your throat. Because of this, they drained the inflammatory process that happened near the lymph node. So, that's what you see when you are on the phone. pag namagaang ipin nyo, usually makakita kayo ng kulani sa leeg.
So this is the reason why. Pero also this organ can cause inflammation. So when you say lymphangitis, ibig sabihin yung lymphatics are inflamed.
So nakakaroon na inflammatory process sa lymphatics. And when you say lymphadenitis, meaning there's an inflamed lymph nodes. Okay? merong single lymph node na merong inflammation therefore we call them lymphadenitis so again when you say lymphangitis there's an inflammation of the lymphatics but when you say lymphadenitis there is an inflamed lymph nodes Okay, if you want to ask, it's okay. Because this is a bit long.
Is there anything you don't understand? Sorry, I'm recovering from pneumonia. Okay, now we'll go to leukocytocrutement, to the site of inflammation. So, we said earlier, the process.
will be recognition, vascular, visodilatation, permeability. So, ito na. So, ngayon, paano naman siya pupunta dun sa area of injury?
So, this step is the key function in the elimination of the offending agent. So, in this step also, it destroys the bacteria, the microbes, or any offending agent that causes injury. And... the important leukocyte for eliminating agents that are capable of phagocytosis are the neutrophils and macrophages again the predominant cell in acute inflammation is your neutrophils also okay but also they could you could also see presence of macrophages in the tissue and or what we call monocytes monocytes these are macrophages that are seen in the blood but if you say macrophages ito yung mga monocytes na pumupunta sa area sa main tissue so it will be activated so and will now cause uh will now uh do phagocytosis pero pag tinanong kayo what is the predominant cell in acute inflammation it is phagocytosis now we'll go to the emigration and accumulation so first is the addition to the endothelium so there are different steps in the leukocyte addition first is imagination margination stasis ruling in addition so later on i will discuss this one by one the next one will be migration to the uh across the endothelium so ito yung they will be able to pass the blood vessel wall. And then the next one, if they have already passed the endothelium or the blood vessel wall, this is what will happen, will be the chemotaxis or this is the direction of the leukocyte in the area of injury.
So what are now the steps in leukocyte adhesion? So first is margination and stasis. So imagine, This leucocyte adhesion is like throwing a coin in a still river.
In water, right? So what will happen first? It will go to the water. So that's the margination. So because of the wall shear stress, there will be a decrease in blood flow.
It dilates, decreases blood flow, accumulates. So these leucocytes will go to the wall. okay so imagine you know again i am too big i am coin pagina guess so put a salas a sata big so this now will lead to the leukocyte assuming the the periphery along the endothelial surface so sorry oh well a cassia home arrow nicole and company go a meta arrow dito anyway so come I keep on you don't neutrophil not all in the picture Nagpunta siya sa periphery, doon sa endothelial surface.
So, it is what you call margination and stasis. Okay? Next is rolling. So, diba, hinagis niyo yung coin.
Ano mangyayari? Nagro-roll doon sa water. So, these steps are mediated by selectines. And they are actually enhanced or like...
the ligands or the enhancers are regulated by cytokines so important cytokines and also selecting in this uh in this um steps okay so if you can see the l selecting the receptor forming your um uh producing your rolling of the leukocytes so what happens this leukocytes will now roll along the endothelial surface so again margination pupunta sa area sa endothelium and then after pagpunta nun so nagkakaroon ng decreased blood flow pupunta sa endothelial surface and then magro-roll because that are enhanced or mediated by selectines and cytokines and after rolling there will be now addition of the leukocytes to the endothelial wall so at certain point itong rolling nato magiging mabagal So, what will happen now, it will now assume the periphery and it will now bind to the endothelium. So, this now is mediated by your integrines and your E-selectines. Okay. So, there are actually different types of selectines, right?
There's L, there's E. So, but I will not ask that anymore. Don't worry.
So, Ngayon, nag-adhere na siya sa wall. So, anong next na mangyayari? Mag-migrate.
Magka-transmigration. Lalagpas na kayo sa blood vessel wall. So, paano nangyayari dito? So, there will be leukocyte recruitment in the post-capillary venues. So, this process is where, when the leukocyte migrates towards the chemotactic region and accumulates in the extravascular side so they are also stimulated by chemokines and also to add at the moment leukocytes at the moment neutrophils at all they also attract other leukocytes okay so hindi lang sila or the cytokines that they release hindi lang sila to mediate rolling margination also to attract other leukocytes.
So, para sila mga, ano tawag din, pag nag-aaway, yung mahanap ng kakampe, ganun, ng kinukuyog nila. So, mag-a-attract sila ng mga ibang soldiers to go to that area of injury. So, what happens in migration?
So, merong addition molecules, you call the PCAM-1 or the CD31. So, they are involved in the migration of leukocytes. So, did they get sila after nilan the mickey so kailangan mag migrate deba so they will now release collagenases so these are enzymes that help pierce the basement membrane of the blood vessel or the endothelial surface um and after that so the peers know nila ngayon ngayon pano sila ngayon papasok o lalabas ng blood vessel wall so merong tumang mga leukocytes na to na mga hair like structures what you call the philopodias so ang ginagawa ngayon ng philopodias pinupol nila yung sarili nila palabas doon sa blood vessel wall so from didikit sila ngayon because of the pkm1 and cd31 What will happen is that collagenases will release enzymes to destroy the basement membrane or endothelial membrane.
Now, they will come out. How will they come out? Of course, that area is tight.
So, they will decompose themselves using their philopodias. Okay? Is that clear?
Yes, doctor. Okay, so nakalabas na sila. So ito yung summary ng recruitment of leukocytes. So hindi ko na-discuss, tumatagal. Okay, next.
So nakalabas na sila ngayon sa blood vessel. So what happens next will be chemotaxis. So what we mean by chemotaxis?
It is the locomotion along the chemical gradient. So meaning, paglabas na sa blood vessel, pupunta siya ngayon dun sa area of injury. So, ito yung tinatawag na chemotaxis. So, these are the movement of leukocytes in the tissue towards the site of injury.
So, there are also chemoattractants. So, it can either be exogenous or endogenous. So, dapat meron mag-attract sa kanila. So, when you say exogenous, pwedeng microbial products or bacterial products yung naka-attract dito. Or...
it can be endogenous using your mediator such as iv such as your cytokines um complement system or complement activation could also be an endogenous chemotaxis agent or it can also be another um media what you call your uh arachidonic acid metabolism so the nature um in of leukocyte infiltrates varies in the age so again the predominant cells are your neutrophil but you could also see monocytes or macrophages again when you say monocytes these are macrophages same as macrophages but this is what you see in blood when it comes to macrophages they are seen in the tissue okay so you will notice that whatever the leukocyte is it varies with the age of inflammation But when the inflammatory reaction changes, you can see that there is a predominant volume of neutrophils, which is the most form of acute inflammation. This infiltrate usually increases during the first to 24 hours. So, it's important to have a timing. And they respond rapidly to chemokines and undergo apoptosis within 24 to 48 hours.
Why? I said earlier that in any mechanism, there should be a regulation. Because they are continuous. For example, this Nutri-Fill, Sodial of the Body, normal tissues can be damaged. They don't have overstimulation.
So, there should be a regulation. So, they undergo apoptosis within 24 to 48 hours. It's also important when it increases. So, in the first 6 to 24 hours. Why?
For example, the patient had a fever. During the onset, the patient usually does not get the complete blood count. So you have to wait. after six hours because that's where you can see the peaking of neutrophil or leukocytes if there is inflammation okay next we'll go to monocytes so they persist longer and they proliferate in the tissue so now we'll go to the process of eliminating the agent or the offending agent so what's the process? so in an inflammatory reaction the mean process of eliminating it will be phagocytosis so inflammation and the mangyari so tapas at idunsa recruitment, it's already there, it's already there in the site of injury.
So what will it do now? It will now activate phagocytosis. So again, in any process, there should be recognition. So it should be recognized that we have a microbe, we have an offending agent.
Next will be engulfment, these are the things that the offending agent is eating. And lastly will be killing and degradation. so in recognition they use they uh usually recognize mannose receptors so uh these are um this mannose receptors they usually bind to the manuase or the focus uh which are remnants of the sugar remnants of the glycoprotein and glycol lipids of the microbial cell wall so you mannose receptors they attract them to the sugar remnants of the microbial cell wall. For example, bacteria. So that's where they attract them.
It could also be scavenger receptors where molecules bind and mediate endocytosis of oxidized or acetylated LDLs. And it could also be recognized by obstinance. so what are obstinance they bind to the microbes to further enhance phagocytosis so there are different types of phagocytosis and more common or commonly used are your crps or lagging must man malaginia marine leg are your c-reactive proteins and also your serum amyloid a um c-reactive protein actually uh some of um they usually request crps if they're considering sepsis, inflammation.
Kasi nga, lumalabas ito in phagocytosis. So, itong mga CRPs na ito, they're optionins pala. So, it enhances phagocytosis. So, pwede itong imeasure during an inflammatory reaction.
Next is engulfment. So, narecognize na ngayon. Ano na ngayon? Engulfment.
kakainin niya ngayon. So makikita niyo to dun sa unang picture sa mataas na picture para nakakaroon ng bibig so they are called your pseudopods so ang nangyayari these phagocytic cells they extend their cytoplasm forming a mouth so for example, meaning they flow around the microbes so So, what happens is, he will eat it now. He will engulf these microbes now. So, when it formed, when the pseudopods, these microbes, these offending agents, these are now what you call your phagosomes. Okay?
So, how can it die? It was just trapped. So, how can it now? um so what happens now the lysosomes this are um part of the cell that contains digestive enzymes different substances that can cause degradation of any of any agent So, these are the fightings. These are the digestive enzymes that can kill microbes.
So, what will happen is, these lysosomes, these are the orange circles inside the cells. So, you can see, it will stick now. So, it will stick now to the phagosome. So, it will now be called your phagolysosome.
So, now, when these lysosomes stick inside the... phagosome, it will release its digestive enzymes. It will have oxidative burst.
It will have a reaction. It will kill these microbes. Okay, so this reaction also is very important in There are certain bacterial infection that will not form.
So one good example is your tuberculosis. So in tuberculosis, initially there is no formation in the first exposure of the person to tuberculosis. In the first exposure, there is no formation of phagolysosome. meaning, the lysosomes don't stick to the phagosomes. So, what happens is that the microbes contain phagocytic cells, but they don't die.
So, what happens is that there's a multiplication of bacteria. But since tuberculosis is a delayed time of immunity, or delayed type of immunity, so after four weeks, there's only reactivation. That's all.
magkakaroon ng activation or magkakaroon ng maturation ng phagolysosome. So hindi naman sa lahat. One good example lang na ito hindi nangyayari initially ay sa tuberculosis. Pero in any injury or any inflammatory process, dapat ito yung normal na mangyayari para malabanan yung mga injuries. okay so after the tonic oxidative burst so i know tomorrow oxidative burst not also in the landman digestive enzyme and lemon and lysosome or and nearly release the lysosome you could also see ros or your reactive oxygen species citric oxides that are also used to degrade or aids in the degradation of microbes So after that, when it dies, it will have exocytosis.
So it will now release phagocytic cells. So that's where the cellular debris will come out. So it will now come out.
So this is what you see in the uterus, right? So usually, the uterus, the exudates, what did I say earlier? It has a lot of proteins. So these proteins are the leukocytes, these are the phagocytic cells. And cellular debris.
eto yung product ng phagocytosis. Okay? So, yun yung mga nakikita nyo sa nanay.
Malinaw? Okay. So, again, eto yung mga nakikita or laman ng lysosome that aids in degradation.
So, it's the reactive proteins. and also nitric oxides and also lysosomal enzymes or your digestive enzymes so uh so these are what they're called the leukoside mediated injury so first it can cause collateral damage because they're not killed by tuberculosis so it causes prolonged host response in tuberculosis and also in certain viral diseases. Another mediated injury when an inflammatory process is inappropriately directed against the host tissue as in certain autoimmune diseases. So sabi ko nga kanina one good example is rheumatic heart disease. Pwede ding acute glomerulonephritis in kids.
So usually pwedeng nagkasugat lang, nagkaroon lang ng tonsillitis, and in a few days, in a few weeks, it can lead to heart disease, rheumatic heart disease, or it can also lead to bleeding in the nose. So, it can lead to acute glomerulonephritis. So, it is caused, this are caused by an inflammatory response. Okay, another one, when the host reacts excessively against a usually harmless environmental substance. So it's an autoimmune response, an immune response.
Meaning, for example, you're exposed to a virus, the patient has asthma. So if you have an allergen, so you will have an allergic reaction. So all of this are your leukocyte mediated injuries. So these are your examples of your leukocyte-mediated injuries. Again, as I said earlier, glomerulonephritis, asthma, atherosclerosis is also one.
Don't worry, I will give you a copy of my lecture in PDF, so I'll give it to the secretary. Okay, now we'll go to the termination. So, kailangan i-terminate, kailangan i-control ang response.
So, this is due to mediators of inflammation that are produced in rapid burst only as long as the stimulus persists. So, dapat ganon ang inflammatory response. If there is a stimulus, there will be a rapid burst.
So another one to control it is, usually, if you notice, neutrophils are short half-lives. So they are degraded immediately. So there is an apoptosis immediately after the stimulus. Okay, now we'll go to the regulation of inflammation.
May I ask about acute inflammation? It's good to read on cellular injury because that's what you'll understand about acute inflammation. Do you have a question?
Answer so we can finish quickly. None, doctor. None? Okay. Remember the regulation of acute inflammation that I will talk about.
You don't have to anyway just give a brief discussion. So what are the features? They are most important mediators and these are your vasoactive amines, lipid products, your cytokines and also your complement products.
They are secreted by cells or generated from plasma protein. They produce only in response to stimuli. They are short-lived and can stimulate release of other mediators. I said earlier, in immigration, even these neutrophils, they have cytokines that are released.
They are attracted by cytokines and these cytokines also attract other mediators to have a cure. Remember this power point. So, when we say histamine, what happens when histamine is released? They usually causes vasodilatation, increased vascular permeability, and endothelial activation. While your prostaglandins, it causes vasodilatation, causes pain, and also fever.
Remember. Leukotrienes. um uh increased vascular permeability they are usually increased leukotrienes they are usually increased in asthma and allergic reactions okay uh anyway next so what are your vasoactive amines your histamine uh they are produced by the mass mass cell base of base of his in your platelet so it causes dilatation and also increase permeability serotonins they're platelet and certain uh endocrine uh neuroendocrine cells and it is faced due to during platelet release reaction so what are your arachidonic acid metabolites so eto yo mga prostaglandin thrombocenes and oxalucutrienes so they are from the cellular membrane phospholipase so it will now reacted by your phospholipases to produce arachidonic acid.
So, inflammation usually gives steroids to the patient. So, this is what steroids target. This is phospholipases. Okay?
So, if there are no steroids, there is a production of arachidonic acid. So, in arachidonic acid, it can produce cyclooxygenases and your lipoxygenases. when you say lipoxygenases it is the production of leukoterines which are usually seen in um asthma okay while your cyclooxygenase target cox-2 cox-1 inhibitors aspirins so ito yung tina target niya ng mga NSAIDs na to ito yung mga cyclooxygenase so it produces prostacyclin thromboxane and your pdg and also the PGE.
So, what is the cost of prostacyclin? Why? If there is prostacyclin, it causes vasodilatation, inhibits platelet aggregation.
Usually, patients can bleed easily. While, traboxyls can also cause vasoconstriction. Vasoconstriction.
Okay, so remember this. Vasodilatation by... caused by prosaglandin vasoconstriction thromboxane increased vascular permeability and the rest are caused by your leukotrienes so prosaglandin so at the cyclooxygenase they are targeted by your cox-1 and cox-2 inhibitors so um they are involved in the pathogenesis of pain and fever in inflammation okay so is and pain and fever next is leukotrienes um uh they are more potent so mass potent shanama cost of bronchospasm in asthma than your histamines so hindi lang histamine and cocos nam pagsisikip ng ng bronchus asthma pwede rin mga leukotrienes okay and your lipoxins which are also inhibitors.
These are your inflammation inhibitors. Other mediators are your ROS, nitric oxides, and your cytokines. So ito yung cytokines. Tandaan. Well anyway cytokines are your interleukin ones, cytokines.
or your interferon gammas so it causes different actions in inflammation. Now we'll go to the complement system. So the complement system in brief there are three reactions.
First I'll go to the classic pathway. The classical pathway yung nasa gitna. It is triggered by binding of C1 to antibody that has combined with an antigen. So classical pathway, merong antigen-antibody reaction. While your alternative pathway, it can be triggered by a microbial surface molecule.
So yung alternative pathway, hindi kailangan na antibody. So they can be triggered or activated. even in the absence of any antibodies.
Pero merong presence ng microbial surface. Ano itong mga ito? It can be an endotoxin, your lipopolysaccharides, or your complex polysaccharides, or your sugars. So pwedeng ang alternative pathway triggered ng microbial surface. Yung classical pathway, merong binding of C1 to an antibody.
So magkakaroon ng antigen-antibody reaction. While your lectin pathway, the plasma mannose binding lectin, it binds to the carbohydrates on the microbes and directly activates the C1. So, magbabind muna siya sa carbohydrate na microbes and then it will go activate C1.
So, all of this complement system will lead to... activation of inflammation phagocytosis, obsolescence and that will lead to lysis of cells. Okay now we'll go to coagulation and kinase so this are activation of Hageman factor your bradykinase they causes increased vascular permeability a contraction of smooth muscle and dilatation of blood vessels so this are other mediators and this one I want you to remember. So pag sinabing vasod, ito yung mga reaction ng inflammation and on the other side will be the mediators of this reaction. So tandaan ha, pag sinabing fever, they are usually caused by your interleukin-1, your tumor necrosis factor, and also your prostaglandins.
Pag pain naman, prostaglandin and also radicanins. So, fasodilatation, histamines, and your prostaglandins. increased vascular permeability seen in asthma they are usually secondary to leukotrienes and also histamine and serotonin so what are the outcomes can be complete resolution it can be healing by connective tissue displacement so it depends on the severity of acute inflammation so permanent cells heal Pwede fibrosis or scarring or there could be progression of response to chronic inflammation. So pag hindi na-solusyonan o na-resolve na acute inflammation, then it will progress to chronic inflammation. So there are different morphologic features of acute inflammation.
First one is the fibrous inflammation. So bakit nangyayari ito? Because of the leakage of large cells. So ito yung mga fibrous. formation.
So it is secondary to an increase in vascular permeability that causes fibrogen to pass out of the blood, forming a fibrin in the extracellular spaces. So that's what happens. So this is usually seen in cancer cells. So again, it is developed due to leakage of specifically or especially fibrinogen, which is a large substance. that passes um to pass out the blood and they usually occur or um accumulate in the extracellular spaces next is the puritive or purulent inflammation so aluminum so it contains neutrophils um cellular necrotic cells and edema fluids Next is ulcers.
Pwedeng nagkaroon ng excavation or of large surface of the organ or tissue. So it can be because of sloughing or shedding of this inflamed necrotic tissue. So these are your ulcers.
So the main outcome, again, elimination of the offending agent. and also restoration to normal. So, pwedeng magkaroon ng complete resolution. So, other outcomes, so pwede ding kunyari nagkaroon ng ulceration, ulcer formation, pwede rin magkaroon ng healing by connective tissue replacement. Pero ito yung worst.
acute inflammation does not resolve and it will now progress to chronic inflammation. Can we have a five-minute break? Okay, sorry. Okay, is everybody ready for my next, the second part?
Yes, po, doc. Nakapahinga na ang lahat. Sure. Kala mo ang no, no? Okay, now we'll go to chronic inflammation.
So, chronic inflammation, so it is a prolonged response or prolonged duration. in which inflammation, tissue injury, and attempts at repair coexist in a varying combination. So what are the occurrence?
It is following a non-healing of acute inflammation. If there is persistence of injurious agents or repeated acute inflammation, and they are low-grade inflammation with no acute inflammatory reaction. So, merong continuous exposure kaya nagkakaroon ng persistence ng inflammatory reaction. So, when you say persistence, It happens when a microorganism are difficult to eradicate such as your tuberculosis.
It can also evoke an immune reaction or a delayed type hypersensitivity reaction and it could lead to a granulomatous response. It can also be immune-mediated, meaning autoimmune. So again, it is a reaction that develops against its own tissue. Also, an immune-mediated reaction can also be because of allergies such as asthma or there can be prolonged exposure to a potential toxic agent either endogenous or exogenous.
For example, these lipids, especially in patients with hyperlipidemia, can cause atherosclerosis which is a chronic inflammatory process of the... arterial wall. So there are different cells. There are usually infiltrations with mononuclear cells. And the hallmark for chronic inflammation is tissue destruction.
So ano ang hallmark ng acute? This increased vascular permeability. While in chronic inflammation, it is tissue destruction due to inflammatory cells.
So the body will try to replace the damaged tissue. Again, in acute inflammation, there can be a complete resolution or it can cause scarring or formation of this fibro-connective tissue replacement. fibrosis and also pag may bagong form na cells pwedeng magkaroon ng angiogenesis or production of new blood vessels okay so anong replacement fibrosis at the same time kailangan meron itong mga blood supply so nagkakaroon ng angiogenesis so what are the cells of chronic inflammations first macrophages so sabi natin it can also be seen in acute inflammation so again pag sinabing macrophages they are called the monocytes on your blood on your blood and also macrophages pag nasa tissue na siya so in chronic inflammation ang dominant cell will be the macrophages so anong purpose niya it ingests and eliminates microbes in dead tissue. They secrete mediators, and they are central to the initiation and propagation of inflammatory reactions.
Next is lymphocytes. They are activated T or B lymphocytes that amplify, and also it can cause propagation of chronic inflammation. They could also release cytokines that again promotes leukocytes or lymphocyte recruitment that persist during an inflammatory response.
Sorry, I don't have an actual picture but I think on your laboratory you will see actual pictures of your of these different cells okay. Next is mast cells. So mast cells they are also seen in acute and chronic inflammation especially so acute inflammation if there is an allergic reaction so it releases prostaglandin and also histamine so increases vascular permeability and also bronchospasm in asthma they are usually elevated during allergic reaction and also in parasitic infections. So, tandaan ha, pag meron parasitic and allergic reaction, you will see mast cells or elevation of mast cells and also eosinophils.
Next is neutrophil. So, sabi natin, neutrophil is usually seen, diba, they are short-lived, and they are usually seen in acute inflammation. But, Neutrophils also can occur in chronic inflammation, but there are different, there are certain condition that could cause an increased uh still of neutrophil at the young uh seen in smokers because of continuous smoking continuous exposure to this injury or injure substance it continuously increases or releases food fill in the body so it will be acute on chronic inflammation okay In chronic inflammation, you could also see granulomatous formation. So this is a form of chronic inflammation that is characterized by collection of activated macrophages, often with till lymphocytes.
And you will see on the granuloma, in the middle, you will see central necrosis. It can either be an immune granuloma or immune-negated granuloma or a foreign body granuloma. So there are different causes or diseases that could cause granulomatous formation. So number one is your tuberculosis, leprosy, syphilis, catch-crash disease, sarcoidosis, and also Crohn's disease can lead to granulomatous formation. So you can see this, don't worry, you'll be very much familiarized with granulomatous formation because every topic is discussed with tuberculosis.
So this is where we'll start. granulomatous formation. So sabi ko nga kanina, especially in tuberculosis, it is a delayed type of hypersensitive reaction. So initially, sa phagocytosis, sa initial exposure ng pasyente, walang phagolysosome formation.
So ano nangyari? Multiplication of bacteria, nako-confine lang siya. So you will wait after three to four weeks.
and then macrophages or leukocytes will reactivate because of your INF2s, tall tooth receptors or activation. So macrophages will activate again. So forming your granuloma.
So in granuloma, as I said earlier, if you can see the center, there's necrosis, right? So... around it or surrounding your granulomas are your histocytes, your activated macrophages macrophages are called your epithelioid cells and you can see here you can see the large cells, these are multinucleated giant cells you can see that there is a nucleus in the periphery so these are your for um uh long-hands giant cells so long-hand giant cells or foreign body giant cells uh there are actually two types so later on i will give i will show you that the two types of giant cells so these giant cells they are formed from activated macrophages that fuse together So, when we say Langhans giant cells, you will see that the nucleus that fuse together are seen on the periphery of the giant cell. While in foreign body giant cell, its nucleus is haphazardly arranged. No matter where it is in the giant cell, you will see the nucleus.
So, that is the difference between Langhans and foreign body giant cells. And usually, Langhans giant cells, you will see it in tuberculosis. So, ito yung horseshoe appearance of the nucleus. Okay?
Gets? Mayintindihan? So, lagi nyo yan makikita sa tuberculosis, especially Langhans giant cells. Yung foreign body giant cells, makikita nyo siya sa arthritis, usually.
Tofu stofy formation, makikita nyo rin siya because these are foreign bodies. So, maano siya na... Ma...
mas essential ng katawan as foreign body dito. So, they will now form foreign body giant cells. So, paano siya na po form?
Again, it is from the fusion of your epithelial cells. So, ano ba yung mga epithelial cells? These are your activated macrophages.
So, sabi ko kanina, macrophages, pag sa tissue, pero pag sa blood, they are called your monocytes. Malinaw? Malina, don't worry, malamit na tayo matapos.
Naantok na ba? Ang boring na pag online, hindi ko kayo nakikita. Anyway, so what are the effects of inflammation? So inflammation, kanina pa ulit-ulit ako sa mediators. Pain, vasodilatation, fever, diba?
So systemically, ang makikita niyo sa patiente will be fever. It is the most prominent manifestation of acute phase reaction or acute phase response. It is usually caused by your interleukin.
tumor necrosis factor, prostaglandin. So remember that table, we usually love the effects of these types of mediators. Next, another effect will be increase in acute phase reactants.
So this is what you remember earlier, the CRP and serum amyloid A, your obstinance, which enhances phagocytosis. So, ito rin, tumataas siya. So, kaya nga, diba, sabi ko rin kanina, if you want to confirm an inflammatory process or an infection, doctors usually request for CRP levels. Okay?
Actually, CRP levels or your C-reactive protein in an inflammation, mataas siya. It can also be seen in thrombosis. Mataas siya in thrombosis conditions, infarcts. Especially if the patient has an increased risk to develop myocardial infection, hindi pa man pwede na i-detect. Pag mataas ang CRP at walang infection, walang inflammatory process, sure ka pwedeng mag-progress to sa myocardial infarction.
Okay? Another effect is leukocytosis. Mataas ang leukocyte formation.
So mataas yung mga differentials. Mataas ang neutrophil, lymphocytes, monocytes, eosinophils. And another one, because of an inflammatory process, pwedeng ano? Because diba una, magkakaroon na increase blood flow, then decrease blood flow.
So, nakakaroon na increase ang BP, increase ang heart rate, decrease ang sweating. The patient could manifest with chills, anorexia, and also mali. kaya usually ang patient with chronic inflammation or chronic infection minsan makikita niyo, di ba ang pasyente parang walang ganang kumain di ba because of this cytokines, tumor necrosis factor that can cause protein degradation so minsan ang pasyente pumapayat because of this okay so now we'll go to tissue repair my question is a chronic inflam my question okay so now we'll go to repair so healing so it occurs in two times can be proliferation of the residual cells and maturation of uh the tissue stem cells or in normal cells or it can lead to scar formation or fibrosis or deposition of connective tissues. So proliferation of residual cells and maturation, they are driven by growth factor. And also, they are dependent in the integrity of the cellular matrix.
And also dependent in the maturation of the stem cells. So what are these cells? There are different types of cells or different types of tissue. It can either be a labile tissue, a stable tissue, and also a permanent tissue. So these are important in tissue repair.
Why? Because during injury, when we say labile tissue, even without injury, even without injury, they're continuously proliferating, continuously producing new types of cells. Anong good example will be your skin.
Diba? Lagi tayo nagsha-shed. Diba?
Hindi natin alam. Para tayo aso. So, lagi tayo nagsha-shed.
Kasi continuous ang production ng epithelium ng skin. So, another one is your oral cavity. So, importante to. So, diba? Minsan parang nagbabalat yung bibig nyo.
So, because these are labile tissues. Okay? They're continuously dividing, continuously producing. When you say stable tissue, so again labile even without injury, continuously dividing. or producing new cells when you say stable tissue one good example are your liver your pancreas your kidneys um they only divide uh when there is injury so they are capable of dividing in response to injury pero they can go as much okay pag naubos na siya pwedeng hindi na siya mag produce na new cells so for example liver, di ba ang liver nagkaroon ng injury.
Usually, ano manilaman nyo, merong fatty change, nagkakaroon ng fat cells, nagiging fat cells to, pero it could only go as much. Hanggang sa itong injury na to, hindi na kaya ng liver, it will lead to fibrosis. So, nagkakaroon na ng cirrhosis ang pasyente. So, ito yung mga stable cells.
Again, they are capable of dividing in response to injury. They have a minimal proliferating activity kasi nga magpo-proliferate lang siya, dadami lang siya, pag nagkaroon ng injury, pag nagkaroon ng loss. And stable cells, they usually stay on the G0 phase of cell cycle.
Bakit G0? Kasi ready silang magproliferate pag kailangan. Okay?
Next one is your... permanent tissue what are your permanent tissue your neurons your cardiac tissue so they do not proliferate even if there is stimulus even if there is injury hindi sya dadami so pag nagkaroon ng injury dito for example chronic inflammation nagkaroon ng acute inflammation severe nagprogress to chronic hindi sya dadami pero ano ang mangyayari it will lead to scar formation Pwedeng hindi nga eh. It depends on the condition, the type of injury, and the type of tissue.
So pwedeng magfibrosis, pwedeng maghindi. Pwedeng hindi. Okay?
Pero it doesn't proliferate pag nagkaroon ng injury. Napapalitan siya ng ibang type of tissue. Okay? So one good example is scar.
Okay? Malinaw? Now, we'll go to, so ito yung labile tissue. Again, you're driven by growth factor.
So again, ito yung labile tissue continuously proliferating while your stable tissue. So they stay on the J0 phase of cell cycle. It only regenerate during injury, but it can only regenerate as much. Kasi pag hindi na niya kaya mag-regenerate, it can lead to scarring or fibrous formation, which is not the usual type of liver cell, right? Because the function of the hepatocyte is no longer there.
So it becomes scarred, fibrous. You'll only see fibrosis. So one good example, I said earlier, livers are stable cells.
So if you have an injury, you'll just replace it. So sometimes, if you have an injury, kung narinig nyo merong liver transplant. Kasi nga, it can regenerate.
Pero it can only do as much. Pag hindi na, nagiging serotic na, nagiging fibrosis na. Okay?
So next, we'll go to connective tissue deposition. So it cannot be accomplished by regeneration. So ito yung mga permanent cells.
So ano nangyayari? It will be replaced by scar formation. So there is a combination of regeneration, liver or stable of residual cells and also scar formation.
So what happens in scar formation? So remember, when newly grown, there is angiogenesis. Even in cancer, there is angiogenesis or formation of new blood vessels. So why?
Because it needs to be supplied with new nutrients and oxygen. itong newly repaired areas okay uh there could also be formation of granulation tissue or can be remodeling of connective tissue so there will be maturation and reorganization of your connective tissue or your scars or what is what you call the stable fibro scars so ano naman ngayon ang nag-influence bakit hindi nagkakaroon ng tissue repair so these are the reasons bakit Infection, diabetes, especially in diabetes, kaya ka diba ang mga pasyente minsan napuputulan ng paa. kasi masyadong delayed ang repair. Masyadong delayed ang inflammatory reaction ang tissue repair nila.
So, nagkakaroon ng, kailangan minsan putulin. So, bakit? Nagkakaroon ng delayed or walang tissue repair, pwedeng delayed healing because of prolonged inflammatory reaction or pwede rin increase tissue injury, masyadong severe injury that the tissue cannot repair itself anymore.
It can also be because of a metabolic disease that causes compromised tissue healing. It can also be protein deficiency because healing needs protein. It needs vitamin C to repair. Also, collagen to repair.
So, if there is protein deficiency, vitamin deficiency, and collagen synthesis deficiency or inhibition of collagen synthesis, there can be... problema sa tissue repair repair another one is your anti-inflammatory effects which causes a weak scar pag ang formation ng scar or connective tissue is very weak then therefore you could not achieve a very good tissue repair and also pag may local pressure pag may continuous exposure to injury to pressure hindi siya mag repair okay so there are different types of food healing it can be healing of skin wound by first and second intention and also uh ito is a skin but in parenchymal organs in the heart and the kidney lahat na nasa loob it is by fibrosis so what is healing by first intention healing by first intention is healing pag ang ang wound or ang sira ang wound ay clean and uninfected so ito yung mga clean wounds or they are surgically incised, ito yung mga gagawin nyo pag nagbunot kayo ng impin. Usually, they are healed by first intention.
So, you will see in this condition, there is approximation. And also in first healing, ito yung mga wounds na there is approximation of the edge of the wound. So, it can be approximated. Meron kayo makikita mga surgical sutures.
And... also it can also be seen in wounds with opposite edges so pwede i dikit so they are you uh combined by primary union so in first healing uh uh injury is uh the involved injury is only on the epithelial layer so a mechanism will be regeneration or epithelial regeneration which is comprises of three process again every injury will be relieved by inflammation after inflammation or resolution there will be proliferation of the epithelial cell. Pag stable cell naman there will be maturation of the connective tissue scars.
So again there is una magkakara ng blood clot formation so this clot now will stop build bleeding and this clot will be the scaffolding or the foundation of the migrating cells or the connective tissues. So first of all, when the blood is drained, it's like the blood is drained, the black, so these are your scab formation. But why?
Because of dehydration of the external clot because it has no supply, so it is exposed to the air and dries. but usually when you get hurt, don't remove the scab because it helps in wound healing. So these are the events during first intention. So in the first 24 hours, you will see neutrophil immediately, right? Very abrupt or very fast reaction of neutrophil.
So there will be clearing now because of this neutrophil will be the there will be clearing of the uh by the of the debris by the proteolytic enzyme so there will be increased myotic activity of the basal cells because it will start producing these basal cells so that it will produce and close so there will be migration and also proliferation of the uh cut margins depositing in the basal membrane so after three days uh the neutrophil because after 42 hours it will be replaced by macrophages and also there will be granulation tissue formation and on the third day you will see the presence of collagen already. While on the fifth day, meron ng blood formation, new blood formation or new blood vessel formation or neovascularization. There is also formation of granulation tissue, collagen debris.
Epidermis now could cover the normal thickness of the injured skin. While on the second week, you will see contention of the skin. continued accumulation of collagen and also still proliferation of fibroblasts.
You could also see leukocytic infiltrates, edema, and in this part, nawawala na ito. Itong mga infiltrates na ito, itong mga edema fluid formation, ito yung mga tumor na kanina nga, yung sinabi ko kanina. so nawawala na siya in two weeks okay so at the end of the month there will be scar formation now we'll go to healing by second intention pag sinabing second intention eto yung mga tissue loss or cell injuries that are very severe or very extensive so you will see this in large wound abscess ulceration and ischemic necrosis So repair involved will be regeneration and also scarring and union is secondary union. Because there is no approximation of wound edges, so what happens is that it is secondary union.
So usually, why is it secondary union? Because you can see there are large tissue deficits, large fibrin clots, they have more exudates and more necrotic debris. and it undergoes extensive inflammatory reaction.
So again, large amount of granulation tissues. Why? Because if the ulceration is high, ulceration or tissue deficit, there's a big gap that the granulation tissue needs to fill.
So, to have a new framework. Okay, so the result is greater mass of scar tissue formation. So in this type, the matrix contains fibrin, plasma, fibronectin, type 3 collagen. So in the second week, it will be replaced by your type 1 collagen. Another process will be the formation of wound contracture occurs, especially in healing by second intention.
Bakit? Kasi nga malaki yung area na nasira. So, pag nagkaroon na siya ng healing, nakakaroon ng contracture, parang naninigas yung area.
So, bakit? Nakakaroon kasi ng, hindi niya na... napapalitan yung gap na kailangan pero mas lumiliit siya para kasi lumiliit din yung wound surface yung surface area ng wound mas lumiliit din so it you will see increased number of fibroblasts in this condition and usually it is seen as an initial process of contracture so wounds check um Recovery is because of the excess of collagen synthesis over collagen degradation during the first two months. And wound strength is usually achieved after three months.
So these are the types of healing again. Fibrosis. So fibrosis is referred to abnormal deposition of collagen. and other extracellular matrix component in the internal organ in chronic diseases. So there are also abnormal tissue repair.
So pwede rin magkaroon ng inadequate formation or excessive formation of granulation tissue or it can also be exuberant granulation. So there are different types. One type of inadequate formation is your dehiscence or rupture of wound So it occurs after abdominal injury, secondary to increased abdominal pressure, vomiting, coughing, and ill use.
Especially the patient who was operated on the chin, the doctor will tell them to avoid lying down, to exert too much pressure on the chin because it can lead to wound dehiscence. The wound can appear. especially after first intention. So it is caused by mechanical stress. Next is ulceration.
Ulceration, so it is due to inadequate vascularization during healing. So these are non-healing wounds also forms in areas of defoil of sensation. So very good example are those patients with diabetic neuropathy. So yung mga pasyente na walang nararamdaman, kaya pwedeng mag-costal ulceration kasi may sugat na hindi naman nila nararamdaman eh dahil nga effect ng diabetes. So lalong nasusugatan, hindi nila, di ba one cardinal sign of inflammation is loss of function.
So usually, ang tendency mo, hindi mo magamitin yung area na injured. Pero since menuropathy sila, hindi nila nararamdaman. And especially, and also in diabetes, in diabetics, medyo delayed ang wound healing nila.
So they are very prone to develop ulceration of wound. So usually, itong mga pasyente na to, magkakaroon ng necrosis ng paa, namamatay yung paa nila, nakita nyo mga itim na. So it can lead to sepsis. So walang choice but to remove that area. So nagkakaroon ng amputation.
So usually, pinuputol ang mga paa or legs ng pasyente with DM. Another will be excessive granulation formation. So, ito yung hypertrophic scars.
So, these are accumulation of excessive amount of collagen. It is to develop after thermal or traumatic injury involving the deep layer of the dermis. So, hypertrophic scar can be keloid formation. Ito yung sobrang OA na scar formation.
So, pag sinad, Sinabing keloid formation, the scar or the connective tissue formation goes beyond to the boundaries of the original wound. So kung ang wound mo ay maliit lang, it goes beyond. Kung 1 cm lang, mas lumalaki pa pag nagkaroon ng keloid, yung pagkaroon ng tissue repair. So it does not regress. So sabi nila inoopera, tinatanggal, pero hindi.
It can inoopera. tinanggal na excessive fibrosis usually nagkakos pa ulit ng another keloid formation okay another one is exuberant granulation or proud flesh formation so these are secondary to excessive amount of granulation tissue but this type it protrudes above the level of the surrounding skin So, mga gandong condition, dapat tinatanggal. Nakakaroon ng excision.
And, yun. Para hindi na magkaroon ng another exuberant granulation formation. And the last one will be contraction. So, diba nga, lumilitang wound because of fibrosis.
Pero there is exaggeration, it is contraction, it is the process in the deformity of the wound and the surrounding tissue. So they are usually prone to develop in the palms of the hand, the soles, and the anterior aspect of the stomach. They are commonly seen after serious burn injury. So, diba, minsan nakikita niyo pag nasunog yung balat ng pasyente. pag hindi siya maayos na na-heal, it can lead to contracture.
So, parang nagdidikit-dikit yung mga skin nila. Okay, do you have any question? That's my lecture. Medyo mahaba.
Akala ko mapapabilis.