Hello, I'm Ms. White and we will be discussing pathophysiology. Today's chapter will be focused on inflammation and tissue repair. So here are our learning objectives for chapter three. We want to differentiate among the three lines of defense. We want to outline the process of acute inflammation including the role of chemical mediators.
We want to describe the process of healing and repair after tissue injury. We want to differentiate between the acute and chronic inflammation states. and also those treatment methods that are used for acute and chronic inflammation.
We want to identify the cardinal signs or clinical manifestations of inflammation and we want to apply those concepts to select clinical models. So we'll start with the lines of defenses in the body and just so you're aware there are three areas of lines of defense in the body. So we'll start with the skin and mucous membranes and then we'll move on to the inflammatory response and finally there is the immune response. So when we discuss the first line of defense, again, this is your skin and mucous membranes. So your skin is this huge organ that helps prevent harmful substances from getting inside of the body.
And again, we have the mucous membranes that also help with that. So when we discuss the mucous membranes, that's normally your eyes, the tears. You have a blank reflex. You have lashes that help catch particles. You have enzymes within those tears that help neutralize harmful substances.
And again, as long as your skin remains intact and your skin is not broken, your first line of defense is intact. So what happens when the first line of defense is broken? Well, we move into the second line of defense, and that's where we have our inflammatory mechanisms or chemical mediators that help fight against disease and infection. So we have two areas that we'll be looking at with that.
So we'll be looking at vasodilation. And we'll also be looking at the chemical response to it, which would include your phagocytes. And once the second line of defense is permeated or is not effective, we move into the third line of defense, which is your immune response.
And again, this is where your immunity cells are activated. The whole immune response is activated and we move on to that very large and plethora of cells that help fight off infection. So if you do have an adequate response at the third line of defense, you end up with resolution of that disease process, which means it does not spread. It means that the body is not affected and that the body was effective at getting rid of said harmful substance or pathogen. Whereas if there is an inadequate response, then that's where you'll see infections and disease spread and things thereof.
So again, your lines of defense in the body are very helpful. It helps protect the body overall. And when those lines are broken, that's where you'll see the progression of moving from the first to the second line of defense to the third.
And hopefully once it gets to the third, if it makes it there, you have resolution. If not, then we have those pathological responses of disease spread. So here we're discussing when that first line of defense is broken, we move into the inflammation area or the inflammation response. So this is your second line of defense. defense that is activated so this is called your vascular response and normally it's in response to some sort of tissue injury and there are three goals of this inflammation response you want to have vasodilation or increased blood flow to the site of injury you want to have permeability where the cells that are involved with healing help get to that site of injury through permeating the epithelial cells and then we want to prepare the area of injury for tissue repair.
So again, the goals of the inflammation response are to have vasodilation, are to have permeability to help with those healing cells to get to that site of injury and then help promote tissue repair or prepare that site of injury for repair. So we will be talking about the acute inflammation response and here is a concept map that will help. I've developed these topics for you. So as you can see, it starts with tissue injury. And once you have that break in the skin or maybe a cut on the finger, this is the response that happens as a result of that.
So once tissue injury happens, we have the production and release of inflammatory mediators. And when we do talk about chemical mediators or inflammatory mediators, those are generally the same term and we just use them interchangeably. When we start breaking this down further, we go into the two branches, which you'll see here as vasoactive mediators and chemotactic mediators. Again, these are two types of inflammatory mediators or chemical mediators that help with the acute inflammation response.
So here we are going to discuss what happens when that first line of defense is broken. We are at the point of inflammation in the body, and again, this is acute inflammation. So this is happening as soon as that injury occurs, the body is mounting this response to help protect itself from harmful pathogens and things that would make the body have a disease process that will spread.
So when we discuss tissue injury, we are looking at two different branches of the inflammatory response. We have the basal act. side and then we have the chemotactic side.
Right now we are going to discuss the basal active side. Anytime we discuss basal active you can bet that we're talking about the vascular response or blood vessel response to injury. And what is occurring here? Well once that tissue is injured we activate the inflammatory response and different compounds are circulating throughout the body to help go to the site of injury. Some of those compounds include histamine, leukotrienes, and prostaglandins.
Histamines is a neurotransmitter, and it helps directly with that inflammation response. It helps to cause that vasodilation and capillary permeability we discussed earlier in this lecture. We have leukotrienes that are produced by leukocytes, which is a type of white blood cell.
And again, these are circulating as a response to that inflammatory activator. We also have prostaglandins, and those are another type of compound, and they specifically help with clotting at the formation, well, clotting formation at the site of injury. So what are the goals of these mediators acting? Well, the goals are to help increase blood flow to the site of injury.
Once we have these histamines and leukotrienes and prostaglandins circulating, we're trying to dilate those blood vessels to help. get more blood flowing to that site of injury. When we have more blood flow to the site of injury, we can have this process called phagocytosis that occurs, which is where cells that help eat or engulf harmful agents are directly shot to that site of injury.
We also have that, those vasodilation that helps with tissue healing. So, When we open up those blood vessels, we're trying to shoot everything that we can to that site of injury that will help with the healing process. So again, we have those cells that help with phagocytosis.
We're also starting the process for healing because it is indeed an injury at that site. And then we have the increase of blood and fluids that helps dilute those harmful substances. So not only are we having that process of phagocytosis that's eating those harmful agents or engulfing those harmful agents, agents but we have blood and fluids that are helped dilating that harmful substance so it's not causing as much injury so again when we have the vasoactive inflammatory response it is a response to tissue injury and we have we do see that blood vessel dilation we do see that permeability and also we see a clotting cascade remember I discussed that there are prostaglandins and those help directly with the clot formation When you have injury, you want to promote healing. Healing occurs when you have clots and you're starting to clot off that area. And again, you want to have that release and continued circulation of those inflammatory mediators until resolution has been achieved.
Here we're diving further into that vascular response. And again, we have cells that help with this inflammatory process as it relates to the basal dilation. So Again, when we vasodilate, we have different types of cells that go to that site of injury. We have the white blood cells that I've mentioned, the leukocytes. And again, they're releasing those leukotrienes to help with that healing.
We also have platelets that help with clotting. And then we have damaged endothelial or damaged tissue cells. This is sending a direct message to the body saying, hey, activate more platelets, activate more clotting factors.
so we can help heal this process after we get the pathogens out of the body. So again, the body is doing this simultaneously over and over and over again to help with healing and tissue repair. So we're still in that vasoactive section of our inflammatory response. And I mentioned that there are different things that are active. reactivate it as it relates to that inflammatory response.
What I would like for you to know is that there are different systems that are also associated with the inflammatory response. And more specifically, these are dealing with that vasoactive area. So you have that complement system, and it is triggered by the presence of microorganisms.
We have that inflammatory cascade that is occurring that helps to destroy and remove organisms. And we also have the process of opsonization, which is the process of making bacteria. vulnerable to cell lysis or cell death. We have the clotting system and again this helps support coagulation or suppress coagulation at the site of injury because you don't want to keep having coagulation after a certain point the body has had enough coagulation at that site of injury and you have to progressively suppress that process.
And then we have the Kynan system and that helps to further and amplify that inflammatory response and it helps to trigger other potent inflammatory mediators. So what I would like for you to know about this slide is that we have this very mass and even though it's a very small cut or you have a very small injury all of this is happening to help start the healing process within the body. The first goal is to one remove those organisms that could cause disease and infection.
and make the individual sick. And then after we clean that up, we have the system that's starting to help repair that area. So again, we want to have this acute inflammation response and just understand that it is a massive response when it comes to the vasoactive side.
So here we're moving on to the other branch of our tissue injury and inflammatory response. Again, this is a part of the acute inflammation response and we just discussed the vasoactive mediators as it relates to acute inflammation so now we're going to talk about those chemotactic mediators and What this does is that they help with the actual process of cell migration To the site of injury, so we're not necessarily working with the vessels themselves We're working with how do we get the cells to that site of injury? So there is a process called chemotaxis, and that is literally the process of moving cells to the site of injury.
And that requires these chemical mediators or chemotactic mediators to help stimulate this process. So once we activate these chemotactic mediators, they are called chemokines. They stimulate a cellular response to say, hey, cells, we need you to go to the site of injury.
So once the cells are activated, there's a process called chemotaxis. Adherence, and this is the attraction and binding to chemotactic cells to the site of injury. And again, this is regulated by overall inflammatory mediators, so you will see a little bit of crossing over when it comes to how the inflammatory response works.
So once those cells are activated and we have adherence, we have the process of migration. So that's where the cell is literally moving in between those endothelial... endothelial cells to help get to those sites of injury. So again, this is the area of injury and we're moving to the site where the injury has occurred. So those endothelial cells literally separate or spread apart.
This process is called diapodesis. When they spread apart, that helps with the migration of the cells that will further help with that site of injury. Once we get those cells to the site of injury, We have a process called phagocytosis.
And what phagocytosis is, is that whatever is harmful in that tissue at the site of injury, those cells will actually engulf or eat those pathogens or those harmful organisms that could potentially cause infection and harmful diseases. So again, we're working with the area of tissue injury when it comes to those chemotactic mediators. We're literally spreading those cells apart.
and getting the necessary white blood cells to the site of injury so we can have phagocytosis and eventually the engulfment of those harmful elements. Again, we have acute inflammation and when we talk about acute inflammation we'll see more platelets and mast cells and PMNs and those are all collective terms for white blood cells. And then we have chronic inflammation. When we look at chronic inflammation we still have this chemotactic response this chemotactic cellular response but instead of seeing those PMNs and platelets and mast cells we actually see macrophages and lymphocytes going to that site of injury because it's happening over and over and over again so the difference between acute inflammation is that we have at the cellular level PMNs platelets mast cells going to that site of injury whereas with chronic inflammation we see macrophages and lymphocytes going to that site of injury. But the process by which they travel there is essentially the same.
We have that chemotaxis, adherence, migration, and phagocytosis. So here we have our clinical manifestations of inflammation. We just talked a lot about what happens at the cellular level when it comes to the inflammation response, but all of that is happening at the cellular level and we can't always see those cells.
So what we're looking at in the clinical setting is the cardinal signs and symptoms of inflammation. The signs and symptoms that are listed on this slide are local or site clinical manifestations or site signs and symptoms of... inflammation and you can see this with the acute inflammation response so you'll have heat at the site of injury you can have incapacitation or otherwise known as the loss of function you can have pain you can have redness and you can have edema these are all the five cardinal signs of acute inflammation in the human body Just like we have local signs and symptoms or clinical manifestations of inflammation, we have actual systemic or full-body clinical manifestations of inflammation. So what you'll see is fever, and that's one of the telltale signs that someone has an inflammation response or some sort of infection. And then you'll also see increased circulating leukocytes or plasma proteins.
And a lot of this... Section will come from your blood test or diagnostics used to detect acute inflammation. Okay, so here are our diagnostics or blood tests used to help detect acute inflammation and the response thereof.
So we have the white blood cell count and the differential. And across the board, if you see an increase in your white blood cell count, that means there is some sort of infectious process going on and the body is developing more white blood cells to help. fight off that infection.
We have the ESR or the erythrocyte sedimentation rate and this is the rate at which red blood cells settle to the bottom of a test tube. Normally an increase in the rate means that there's more red blood cells circulating, there's more blood flow to the sites of injury or inflammation to help with healing. We have C-reactive protein and this is something that's produced by the liver.
And when the liver produces more CRP or C-reactive protein, that means that there's an infectious process going or some sort of inflammation response. We have the complement activity and it measures the amount of complement proteins. Complement helps to fight pathogens. So if you have an increase in your complement activity, that means the body is trying to fight off more infection. We have prothrombin time.
And this is a value that measures the time it takes for a blood clot to form in a cephal. So if there is a low time, that means you're at risk for developing blood clots. And if it's high, that means you're at risk for bleeding. When you have the fibrinogen test, this is also a test that looks at blood clots.
But when you have a high value of the fibrinogen, that means that there's too much clotting and you may develop a blood clot. clot that is dangerous such as those that would you would see in strokes or things of that nature in the heart when it's low that means you're not clotting enough which means that if they were to cut on you for surgery or to make some sort of incision that means that you're at higher risk for bleeding so again these are different tests that are used to detect acute inflammation. And please note that not one test just tells the whole story.
You get a pretty good idea if you have a variety of these tests on an individual and it helps give you a better clinical picture. But just kind of understand what happens when which diagnostic is high or which diagnostic is low and what happens or what does that tell us when it relates to the body. So now we're looking at treatment of inflammation and these are just generalized goals for the treatment. of inflammation. After a certain point, inflammation does become painful and it is tedious to deal with for that individual.
So you want to help reduce that process as a treatment plan. You don't want the body to overproduce or overdo the inflammation response because too much of that inflammation response can cause issues as well. So what you want to do is help to reduce the blood flow. You want to decrease the pain at the site of injury.
You want to help to block those actions of chemical mediators and you will want to decrease the swelling at the site of injury. So when we're talking about those goals that we listed previously, the reduction of blood flow, the decrease of swelling and pain, and blocking the action of those chemical mediators, we do have non-pharmacological methods that help with that as we reduce inflammation. So you want to use something called the RICE method and RICE is Rest ice compression and elevation. When we rest that site of injury it helps prevent further injury and allows the body time to recover.
When we use ice It helps to decrease that pain through numbing of the affected area and it also helps slow down and block the action of various inflammation mediators. When we have compression, that helps control that swelling in the site of injury and it also helps to reduce that blood flow to that area. And then when we elevate that site of injury, it also helps to control the swelling and reduction of blood flow to that area. So when we use the RICE method, it's to help calm down that inflammation response because it should have done everything that it should do for that individual.
And now we're trying to scale it back so the individual is not uncomfortable as they are healing. There are additional non-pharmacological methods to healing and to treat inflammation. You want to use warmth and heat once everything has settled.
You want to have gradual increased movement. You want to have optimal fluid intake and optimal nutrition intake. We discussed non pharmacological methods to help with inflammation so now we'll talk about pharmacological agents that help treat inflammation and Some that you may notice are insets and that's generally you're paying analgesics you're paying medication you have glucocorticoid steroids, which are medications that help with the inflammation process and then you have aspirin that helps with those platelet factors. So again, you have pharmacological agents that help treat inflammation and help reduce that inflammation response. So now we're going to discuss the concept of healing and tissue repair.
This concept map falls in the place of the acute inflammatory response happening, that site of injury occurred and that first line of defense has been broken. Now we have that acute inflammatory response. And now that the Inflammatory response has come and it has worked. Now the body is preparing to heal itself. So we have different phases of healing that we are going to discuss.
We have the inflammatory phase which helps with the acute inflammatory response and this is where we see the sealing of the wound. And then we have the proliferative phase which is where we have the cleaning up of the debris and the harmful agents that are within the body. Again, this is the area that helps clean up.
We have those macrophages, we have those PNMs, those polymorphonuclear neutrophils, and then we remove the tissue that is dead in the proliferative phase. Again, this is helping to clear all of the debris and those harmful agents that would cause infection and disease. And then in the proliferative phase, we want to help restore that structural integrity.
So you'll see... rebuilding of those tissues that were that either have become necrotic or have become damaged so you'll see a provisional matrix that's just your starting point you'll see granulation tissue you'll see where the body is starting to rebuild that extracellular matrix and you'll start seeing the rebuilding of that connective tissue so all you should know here is that once everything has been cleaned up that debris has been cleaned up the body is starting to restore that structural integrity within the proliferative phase. And then we finally have the remodeling phase. And this is where functional integrity has been restored.
So do not get this confused with restoration of structural integrity. In the proliferative phase, that's where structural integrity has been restored. When we're remodeling, the functional integrity has been restored.
So again, that's where we have movement in that site of injury again. We have the remodeling of the tissues. We have resolution repair.
We have regeneration. So again, the body is able to move that extremity again after being injured. And then we finally have the remodeling of the cells. We have the degradation of the provisional matrix. So that matrix that we started to see with rebuilding is now fading away and then the maturation of those cells that were once damaged and we had to replace those cells are now maturing into the new cells that will function fully as if nothing has happened to that area.
So again, we have three different phases of healing and tissue repair. We have the inflammatory phase, which is the initial site where we have that injury. That first line of defense has been broken.
We have inflammation. The body has now successfully had an inflammation response. We move into the proliferative phase. We're clearing that debris.
We're restoring structural integrity. And then we have the remodeling phase where we're restoring functional integrity. So again, look at this concept map.
It's a really good review on the healing and repair concepts within this chapter. So in pathophysiology, we're talking a lot about what happens with the body when things go wrong. So ideally, we want healing and tissue repair to be successful, but sometimes it is not.
And we have several different complications of healing as a result. You may see infection as a complication, and that is an invasion by microorganisms or harmful pathogens that help spread disease and infection within the body. You have...
ulcerations where at the site of injury you have open crater like lesions and that is generally an eruption or broken area of that skin or mucous membrane that has ulcer you have dehiscence where if an individual has a wound that has been sewn or has partially healed that wound splits open or it bursts open due to deficient scar formation. So you see a lot of that after surgery, especially in abdominal surgery, you may see dehiscence a lot. But again, that's where a wound that's supposed to be healing, that has supposed to have sealed off, was not successful and it has burst open. You have keloids, which are scars, but they're overproducing a scar, so it's hypertrophic. It is a result of excessive collagen production at that site of injury.
In this picture here, this is actually a keloid. And you normally see this when individuals get piercings in their ears. You have that overscarring of tissue due to maybe lack of care of that site. Maybe that area was not cleaned appropriately. Or even when it did scar over, it became hypertrophic.
became over scarring and excessive scarring and that's where you have the development of this keloid and then you have adhesions and That is connections between serious cavities and nearby tissues. So this is a complication because Certain things are not supposed to have connections but because of inappropriate healing You may see these fibrous connections develop in inappropriate places. So You have infection, ulceration, dehiscence, keloids, and adhesions as complications of healing. Earlier in this lecture, we talked a lot about the acute inflammation response. We talked about the mediators that were involved.
We talked about the manifestations of acute inflammation. We talked about what the body does after the acute inflammation response. Now we're going to move into the chronic inflammation response. And again, Chronic is characterized by inflammation particularly that is persistent over several weeks or longer. So we see this reoccurring inflammation response over and over and over again in the body.
And when we talk about chronic inflammation, more oftentimes than not, we have macrophages and lymphocytes that are involved in the chemotactic area of our inflammation response. When we discuss the... acute inflammation response, we have PMNs, mast cells, things along those lines that help with the acute inflammation response.
But when we discuss the chronic inflammation response, those cells that are occurring and helping with that response are macrophages and lymphocytes. And again, we do see some complications and healing as a result of that chronic inflammation. So you may see some scarring.
granulomas that develop as a result of chronic inflammation. A lot of our chronic inflammation clinical manifestations are listed here. One thing I want to point out and probably is the most important is that it is characterized by remissions and exacerbations. So as we discussed remissions is the reduction of those signs and symptoms and exacerbations is the development or reoccurrence of those signs and symptoms. And a lot of these signs and symptoms may mimic those of the acute inflammation response.
But again, what makes the difference between chronic and acute is the fact that there are remissions and exacerbations with this inflammatory response. You will see fever. You will see malaise, which is weakness.
You have anemia. You have fatigue, anorexia, weight loss, weakness. And again, malaise and weakness, you can use those interchangeably.
But malaise is more generalized weakness. But again, all of these would be manifestations of your chronic inflammation response. So again, with the chronic inflammation response, we have those remissions and exacerbations. So one of the keys with chronic inflammation treatment is long-term anti-inflammatory medications.
So you want to have something that will help treat the inflammation over time because it's occurring over and over and over again. But the thing about treatment is that you want to get to a regimen that helps with remission and prevents exacerbation of that chronic inflammation. So if you could find a regimen or if that individual finds a regimen that works for them, this would be considered a long-term therapy for that individual.
You want to have antimicrobial Antimicrobial therapies for infections. Sometimes individuals develop super infections or co-infections and they need long-term use of antimicrobial therapies for this chronic inflammation and infection. You want heat and cold therapy.
You want immobilization. Dietary changes help with chronic inflammation. Sometimes different foods exacerbate the clinical condition.
You want to help the clinical condition with exercise and physical therapy and of course rest. So here are several examples of the application of inflammation. These are different disease processes that we'll discuss in this chapter and again it's important to note that these are not all of the examples but these are just select few that would be applicable to this chapter.
You'll be completing your disease cards on these topics so it's good to take them out and if you would like to fill them out as we're discussing it in this lecture feel free to do that. So we'll start with sinusitis and generally if you see itis that indicates some sort of infection or inflammation process as relates to that area of the body. So we're talking about acute sinusitis and this is a sudden development of this disease. When we discuss the pathophysiology it is blocked areas of the ostia most often due to allergies viruses or other forms of irritation. What happens is that there is an impaired clearance of mucus by cilia and then when that mucus is not cleared, it causes that inflammation or irritation in that area.
The clinical manifestations include fever, facial pain in the sinus area. You have nasal congestion, excessive nasal discharge, persistent cough and fatigue. As far as your diagnostics, you have to have a physical exam by a healthcare provider.
And as far as your laboratory data, you have to have a physical exam by a healthcare provider. You have your ESR, your erythrocyte sedimentation rate, your CRP, which is your C-reactive protein, and your white blood cell count that will help indicate some sort of inflammation process. And as far as your imaging studies, you'll have sinus radiographs. You can have x-rays or CT scans in that sinus area to determine if there is sinusitis going on. So the treatment for acute sinusitis to eliminate the infection, so if it's due to allergies, viruses, or other forms of irritation, you want to remove those.
You may be prescribed some sort of antibiotic treatment that is compatible with that individual. You may use nasal sprays, antihistamines, that's important because when we have inflammation, histamines are circulating so you want to decrease that inflammation response by prescribing antihistamines and then you want to have a decongestion that will help clear that area of the sinus more effectively. Here we're discussing chronic sinusitis and the pathophysiology is similar to that with acute sinusitis with the exception that you have low-grade inflammation in the paranasal sinuses that last 12 weeks or more without flares of acute sinusitis. So what that is saying is that acute sinusitis can lead into chronic sinusitis or you could just have the same infection for over 12 weeks that developed. It does develop from acute sinusitis that is untreated or does not respond to treatment, and it can also be multifactorial as far as its etiology.
So it could be environmental or genetic influences. Some individuals are more prone to develop chronic sinusitis than others. Clinical manifestations include low-grade fever, facial pain in the sinus region, nasal congestion, excessive nasal discharge, persistent cough, fatigue, anorexia.
You have hypoxia. which is the reduced ability to smell. You have that facial fullness.
You have discomfort, pain, headache, sore throat, foul breath, and an unpleasant taste. And you may also have that chronic cough due to the drainage. Diagnostic criteria includes a physical exam from your healthcare provider and the same laboratory imaging as listed.
You have your ESR, CRP, and white blood cell count. Imaging would include your sinus radiographs, X-rays, and CT scans. And as far as treatment, again, you want to eliminate that infection and you want to have symptomatic treatment.
So you want to care for those symptoms. Antibiotics would be prescribed. You have nasal sprays and saline irrigation, antihistamines, decongestants, glucocorticoid steroids, and surgical treatment. Here we have burns.
The pathophysiology for burns are direct contact with excessive heat, radiation, caustic chemicals, or electricity. It can be severe. And it depends on the type of exposure and the amount of exposure, the time of exposure.
So burn severity is directly correlated with that. And again, as a result, when someone is burned, you have the acute inflammatory response that is started. As far as your clinical manifestations, you have different variations of burns. You have superficial partial thickness burns, which result with heat, swelling, pain, retinus, loss of function.
Those... five cardinal signs of inflammation. When we move into a more deeper burn, the deep partial thickness, you have blistering, redness, heat, pain, edema, and serous exudate, so you have some leakage there. And then with a full thickness burn, you have redness, eschar, edema, and exudate. So when you have your different types of burns, it depends on how deep those burns are, and again, that severity.
correlates definitely with that time and amount of time and exposure within that trigger, whether it's heat, radiation, chemicals, electricity. As far as your diagnostic criteria, you have the rule of nines and you also have the ABA burn severity scale. As far as treatment, you want to remove the source of injury and cool and rinse the skin depending on how severe that burn is.
You want to Ensure that if it is a severe burn and it's diffused throughout the body that you protect that individual's airway, breathing, and then you focus on the circulation. Normally, you'll see in an acute state for severe burn fluids being administered, you'll see analgesics. And as they begin to treat that burn victim, you'll see antibiotics being administered because that's open skin. So that leaves the possibility of infection to develop. and you also want to help encourage nutrition.
And because this is a burn, it will require wound management and you may see some hydrotherapy or skin grafting to help treat those wounds as a result of the burn. Again, that would depend on how deep that burn is and you normally see the hydrotherapy and the skin grafting with more full thickness burns. So here's... slide that details the classifications of burns and again we have the superficial burn which is just on that top layer of the epidermis and that's where we see the five cardinal signs of our inflammation response there when we move to that the partial thickness burn that's where you start seeing that exudate and that leakage and it's Literally in that area below the epidermis.
So not only does it touch the epidermis it goes below that and it starts touching the dermis and that's where we see some damage with the deeper blood vessels here and then when we have that full thickness burn it goes all the way down to the subcutaneous layer so that's that fatty part of the body normally when we have subcutaneous area that's the area that we administer subcutaneous medications right so That area from the top of the epidermis all the way down to that fatty area has been burned off and we see complete damage of those blood vessels. We see complete damage of that dermis area. You'll also see that exudate leaking from the burn and you may see some ex-scar of the skin at that area.
When we classify our burns, there are different... types of classifications. The one that I mentioned in this lecture is the rule of nines.
As you can see, there's a rule of nines for the adult patient, but then when you look at the infant or a baby, you have a different percentage criteria here. So really with the rule of nines, I want you to focus on picture A, the anterior and the posterior, and you'll see that each area of the body, front and back, is worth a certain percentage. And these percentages are based off of the number nine. So four and a half is half of nine.
Eighteen is two times nine. Nine is indicated by the legs. So what you'll do is on the front and the back of the individual, you'll see what areas of the body is burnt. And this is where we get, oh, the patient has a 45% burn. Oh, they have a 71% burn, 72% burn.
All of that is based off of the rule of nines here with this picture. Again, the American Burn Association has designated the criteria for distinguishing major, minor, and moderate burns, and it is based on the wound depth, surface area, and the required level of treatment. But the main point of the slide is to understand the rule of nines and how percentages matter when it comes to burn severity. So here's rheumatoid arthritis in your textbook. it does discuss arthritis as the degeneration or inflammation of the joints, but right now we're just going to focus on rheumatoid arthritis.
So please don't do double work, just focus on rheumatoid arthritis. And this is caused by chronic inflammation of the synovial membranes and synovial hyperplasia. When we talk about synovial, this is an area of the joint. And when we talk about hyperplasia, this is the enlargement of those joints or areas. So When we discuss the pathophysiology, it is chronic inflammation.
So it's happening over, there's exacerbations, there's remissions. These membranes are enlarged and they increase the reproduction rate of the cells. So again, this is the enlargement of the synovial membrane. When we talk about synovial areas, it causes joint erosion and pain. So this is where a lot of that pain happens with patients with rheumatoid arthritis.
and it can be mild to debilitating. It can cause pain, stiffness, symmetrical joints, redness, heat, swelling, and decreased mobility. As far as your diagnostic criteria, of course you're gonna have to have a healthcare provider to diagnose, but there is no definitive test for a rheumatoid arthritis.
But there is an increased likelihood with positive findings of an increased erythrocyte sedimentation rate, increased C-reactive protein. increase in your rheumatoid factor or IgG and that is an immunoglobulin we'll get into that a little later and we have anti-nuclear antibodies as far as your treatment you want drugs that help to induce remission so we want to get to a point where we don't see all these signs and symptoms to the patient you have DMARS which are disease modifying anti rheumatic drugs you have codicor steroids and you have NSAIDs as far as non-pharmacological you want rest and activity, you want splints, you want to have physical therapy exercises and things that will help to decrease pain overall so you can use the rice method in this case as well. So next we'll talk about acute gastritis and of course itis is an inflammation or infection in the area that it's describing so we're in the gastric area the gastric is the stomach. The pathophysiology is that it is caused by the ingestion or the taking in of irritating substances.
And those substances can be alcohol, it can be spicy foods, things that don't agree with your stomach area. Regardless of what the irritating substance is, it does cause gastric perfusion to be poor. It does cause acute inflammation on that gastric mucosa, that gastric lining. And those epithelial cells that make up that gastric lining, necrose, so they are indeed dying. So that's where you'll see different clinical manifestation signs and symptoms.
It can be mild to severe abdominal pain. You have indigestion, acid reflux, loss of appetite, nausea, vomiting, hiccups. As far as your diagnostic criteria, of course, you have to be diagnosed by a health care provider.
You'll have an endoscopic examination, so that's when they're going inside of the mouth, through the esophagus, inside of the stomach, to see how extensive the abrasion is or see how the epithelial cells or that gastric mucosa, how damaged it is. You may also get a stool sample or stool analysis, and what they're looking for is the presence of blood in the stool. And paired with that, they will do a complete blood count.
And they'll look at what they call your hemoglobin and hematocrit levels, which would speak to anemia. If you have that abrasion of that lining in the gastric mucosa, you will bleed. And that's where that blood will come out.
The treatment is to discontinue the ingestion of irritating substances. And then you want to buffer or decrease the production of gastric acid because that's also causing that irritation there. So you may see people take antacids.
proton pump inhibitors and depending on the extent of that acute gastritis sometimes they may take antibiotics. So next we are going to talk about chronic gastritis and again when we talk about itis that is the inflammation or infection of the area that is referencing gastric. So this is in the stomach.
So chronic gastritis differs from acute gastritis in that there is a causinic bacterium or pathogen. That pathogen is called Hikilobacter pylori or H. pylori for short.
And this bacteria proliferates in the gastric area. It lives on the epithelial and mucosal cells and it causes them to atrophy. So again, this is a chronic infection. It ultimately leads to gastric acid production being impaired in the stomach. And when you don't have the appropriate amount of acid within the stomach, you do have these.
different clinical manifestations that occur. So again, chronic gastritis is caused by hakelobacter pylori or H. pylori for short. Clinical manifestations are indigestion or dyspepsia. You have loss of appetite, vomiting, anemia, weight loss, and sometimes it can be asymptomatic if the bacteria has been eradicated enough to not cause a lot of symptoms.
You may have some asymptomatic. chronic gastritis and this would be in the case of there being a remission of chronic gastritis. You have diagnostic criteria, you have endoscopic examinations, you have the biopsy of gastric tissue where they're looking to see if the kilobacter pylori is living on that gastric area. You have the pylori breath test and all that is doing is that you're breathing into a bag. and what that bag does is it helps detect different presence of the kilobacter pylori so you do use it not only for gastritis but you can use it to detect if a person has symptoms for a peptic ulcer disease or gastric cancer so that is a catch-all test but again the goal is for it to detect a kilobacter pylori it also helps detect if the infection has cured so if you receive a certain level or rating when you do the breath test at first and then they treat you, they may do that breath test again to revisit that and see if the infection has been eradicated or at least calmed down.
As far as other diagnostics, you may have blood tests. They may search for protein antibodies, and they also are looking at your hematocrit and hemoglobin to see if you're bleeding. As far as treatment, you have antibiotics because this is a bacterium.
You treat bacteria with antibiotics. So you're going to get antibiotics to help hopefully eradicate the bacteria. You will have proton pump inhibitors that help decrease the abrasion of the gastric acid that's in the stomach. You have bismuth, that's normally your Pepto-Bismol type medications to help line the gut. You may also get immunosuppressive drugs for the autoimmune processes, and then they're always going to replace your vitamins because this is leading to more of a nutritional issue.
They want to make sure you have the appropriate vitamins. So vitamin B12 will be prescribed. So now we're moving into acute pancreatitis.
And again, itis indicates some sort of infection or inflammation response. And we're, of course, focused in that pancreas. So The pathophysiology is that it is caused by excessive alcohol use or it is caused by your biliary ducts being blocked and normally you see gallstones that are the cause of obstruction there. Regardless of which cause, they both cause injury to your acinar cells within your pancreas, the pancreatic duct, and it also inhibits those protective digestive feedback mechanisms within the pancreas.
Clinical manifestations include nausea, vomiting, diarrhea. anorexia and upper abdominal pain and that's just simply where the pancreas sits in the abdomen. So when we look at that abdominal pain, it is sudden in onset.
It grows in the intensity. You can have a dull, steady ache or it could radiate to the back. All of these would be manifestations of that upper abdominal pain. Diagnostic criteria is that, of course, you have to have a health and physical examination and be diagnosed. by your healthcare provider.
Then you have different laboratory testing. We have your complete blood count, where they would check for bleeding, of course, anemia with that hemoglobin and hematocrit. They'll also look for that white blood cell count to be elevated. Your ESR would be elevated here.
Your CRP would be elevated. And then there are two different, or several different types, but two overall types of tests that we didn't talk about yet. We have our pancreatic test, which involves the serum amylase and the lipase. And we also have the liver function test, which includes your alkaline phosphatase, your aspartate transaminase, and your alanine transaminase.
So these are for short called your ALP, your ALP. and your AST. So elevations and all of these liver function tests would indicate some sort of liver dysfunction. With your pancreatic test, the amylase is sensitive to your pancreas, but the lipase is more specific to the pancreas. So they would look for both to see if there's any pancreatic dysfunction.
As far as your liver function test elevations and all of these would indicate some sort of liver dysfunction. But it's important to know that alkaline phosphatase is more specific to your biliary function. And again, it will speak back to that gallstone blockage if there is a blockage in that biliary duct. So you would get all of these tests performed if there's a suspicion for acute pancreatitis. As far as treatment is concerned, you have intravenous hydration.
you want to give analgesics and then if there is a gallstone that is causing a blockage in that duct you want to remove that gallstone surgically so now we're moving into chronic pancreatitis and again you will see some dualities with the pathophysiology of chronic pancreatitis and acute pancreatitis so again we see that cause of excessive alcohol and the extent is that those acinar cells have become so damaged that they're atrophied and fibrotic which leads to a loss of function. You also have that bile duct obstruction. This bile duct obstruction has occurred so long that you have some ischemia or death of cells, which also leads to a loss of function. We also have autoimmunity, and sometimes we cannot tell why it starts from an autoimmune disorder.
However, that etiology would be considered idiopathic because there is an indeterminate cause for chronic pancreatitis. When we're looking at the clinical manifestations, we have diarrhea, steatorrhea, which is a fatty stool. We have weight loss. We have abdominal pain.
And this pain is a little bit different from acute pancreatitis in that it is severe and intermittent. Sometimes it lasts several hours, and it is unpredictable at different intervals. You have diagnostic criteria. Of course, you have to be diagnosed by a health care provider first and foremost.
And then they may opt to do an invasive. procedure called ERCP that is a very long word and you can try to pronounce it I'm not going to do that on this particular slideshow but just know that this is a type of endoscopy and what they're doing is going inside and they're looking to see if their diagnosis is correct but also this procedure helps prepare them to be able to treat that suspicion if they have to go in and remove those those ducts and repair that area So you can do direct aspiration of the pancreatic duct to get rid of those stones that are blocking. And then they will look at your laboratory data.
In this, we're looking at the MLAs and lipase, but they will also look at those liver function enzymes we discussed earlier. They'll still pull that CBC complete blood count to look at everything else prior to doing an ERCP. So once they have determined the cause and have repaired as much as possible, You will see some analgesics. There may be some antibiotics depending on the risk for surgery, if the patient will develop an infection or not. But after that, you will see some behavior modification efforts.
So they will encourage the patient to do alcohol cessation, smoking cessation, encourage exercise, and encourage good nutrition. So again, when we're looking at chronic pancreatitis, It is the extent of damage caused by either etiology of alcohol or bile duct obstruction by gallstones. So now we're moving into our inflammatory bowel diseases. We will talk about two different types in this lecture.
The first one that we'll discuss is Crohn's disease. Now the pathophysiology is idiopathic in nature. That means that we do not have a known cause.
It is characterized by inflammation. and it's chronic inflammation so you'll see remissions and exacerbations of this inflammation in the small intestine. You will see this throughout the GI tract but again Crohn's disease is most commonly found in the small intestine. It is characterized by non-continuous penetrating ulcerations so you don't see ulcerations all throughout they are scattered throughout the small intestines and you will see impaired intestinal absorption as a result.
the area that Crohn's disease affects is the area of absorption, which is in the small intestines. And you can also see some bowel obstruction as a result of Crohn's disease. As far as your clinical manifestations, you have abdominal pain, diarrhea, malnutrition, occult blood in the stool, or you'll see blood in the stool. You have fever, weight loss, and fatigue. As far as your diagnostics, of course, a health care provider has to do a physical examination.
You may have an endoscopy. You may have different CT abdomens. You may have x-rays.
And they will also perform stool cultures. As far as your treatment, you want to manage the symptoms of malnutrition. You want to manage the symptoms of abdominal pain.
So you'll see an encouraging of nutrition. And you may, depending on the extent of this disease, you may see these patients on TPN and lipids just because it helps support the nutritional status of that patient. As far as abdominal pain, of course, we're treating with analgesics for that.
Diarrhea, you can treat that with the antidiarrheal. It is a lot of symptom management when it comes to the treatment. They will encourage dietary changes, low fiber diet, because the fiber would... If it's a high fiber diet, it would increase the status of diarrhea within these patients, and you don't want to do that.
So it will be a low fiber diet and, of course, surgical treatment. As far as surgery is concerned, they may have to place a temporary ileostomy in this area until it heals, or it may be permanent if there's no healing available. So again, Crohn's disease is different in the inflammatory bowel diseases because it mostly affects the small intestine.
So now we're moving into the second inflammatory bowel disease in this lecture and similar to Crohn's disease ulcerative colitis has an idiopathic cause or idiopathic etiology. We know that it is chronic inflammation and normally this one begins in the colon and in the rectum and we see continuous areas of ulceration, perforation, and obstruction. Ultimately if this continues without treatment you can see some massive hemorrhaging. the individual with ulcerative colitis.
Clinical manifestations include diarrhea, rectal bleeding, abdominal pain, fever, weakness, fatigue, and anemia. As far as your diagnostics, of course you have to have a history of physical by a health care provider. You have to have an endoscopy for them to look inside and see the area and extent of damage.
You have different radiographs and that can include CTs and x-rays. You will have a complete blood count to check. for anemia and normally that's with your hemoglobin and your hematocrit and they will also look at your white blood cell count in this disease as well as far as your treatment you want to do symptom management so you want to treat the pain that you're experiencing with analgesics they will have pharmacological treatments with that you have dietary changes you want to have a low fat or excuse me a low fiber diet with it individual with ulcerative colitis because you don't want to exacerbate the areas that are damaged. And there may be surgical treatments.
So instead of an ileostomy, individuals with ulcerative colitis may have a colostomy. And that's one of the main differences between these two inflammatory bowel diseases. So very similar with the clinical manifestations, but just mild differences when it comes to location of inflammation and the perforations and obstruction. This concludes our chapter in this lecture.
Some things I want you to do is make sure you review the book and complete your guided learning questions. Make sure you complete your system disorder or disease cards. Make sure you pay close attention to your case studies and activities that will complete in class.
Make sure you review those disease cards. Make sure you review your guided learning questions and also look into your risk factors. clinical manifestations, pathophysiology, diagnostics, treatment, and the application thereof. And make sure you check your understanding so you can close your self-quiz others, answer questions in the back of the textbook, and then make sure you develop your own questions if you have anything else that needs to be clarified. You are more than welcome to reach out to me.
I am available by email and after class. If you have anything else, please feel free to reach out. Thank you.