hey everybody I wanted to give you guys a quick uh little week one quiz review um that covers uh chapter 1 2 4 and 7 so uh I know we go in a lot in depth in the lecture however I'm going to hit on some key points really uh so understand that pathophysiology is simply the study of the of the functions of the human body in a diseased state right excuse me so you know we talk about like Anatomy it's going to be like the study of the structures physiologist the study of the normal functioning however path is going to be study of the uh functions of the body in a disease State like I mentioned right so when we look at the framework of pathology you have to understand iology right so iology is basically the study of the cause or the reason of the disease right so basically what caused it right that's what we're talking about when we're looking at ideology right now when we look at the different classifications of you know diseases it could be idiopathic right idiopathic means the the causes known right or it could be a otogenic disease right and an otogenic disease is uh a disease caused from the results of you know unwanted or unintended Medical Treatments from for example like surgery um then you have like infectious diseases right um a disease that's going to come from uh some type of infectious agent such as a bacteria or a virus or fungus when we look at risk factors risk factors um are simply factors that when present increase the likelihood of of a disease it doesn't mean that you're going to get it right but it does increase the likelihood of an individual getting a particular disease so when we look at the stages of illness right so remember the stages of illness right and and I'll keep keep it pretty simple um if we're in that latent stage right that latent stage is the time between exposure of your tissue to that injurious agent to the first appearance of signs or symptoms right so in that latent stage right that beginning stage there's no symptoms yet basically okay if it's like an infectious disease then we call that the incubation period so the next stage we have is the prodromal period all right that prodromal stage I guess and so this is the time during which the first signs or symptoms appear indicating the onset of the disease right so these is where you're going to have those early symptoms in PR dromo okay and I'm going to H on another uh stage and that's going to be that subclinical stage right and that's when the disease is present but the the person is not going to be experiencing harsh symptoms okay be mindful of symptom versus sign okay a sign is going to be a objective or observed manifestation of the disease right so you can observe like a fever you can observe uh like a bruise on someone's skin but a symptom is something that's only going to be really felt by the patient right so if I'm the patient I feel fatigue or I feel nauseous or I feel uh I have a headache something like that right so symptoms are what the patient feel a sign is what you can see and again remember these uh stages of illness okay when we look at epidemiology it's just simply the study of the pattern of diseases involving uh populations right so um remember these different types how we're going to classify so we can classify diseases as as an endemic disease endemic diseases are going to be native to a local region right uh then we have an epidemic right and so an epidemic is where that disease is spreading uh to many people at the same time sometimes fast right and a pandemic is basically on a larger scale as many epidemics or an epidemic everywhere basically um similar to like how Co was right it was almost everywhere when we look at the levels of prevention uh and some examples so here are the levels of prevention right we have primary prevention secondary prevention and then tertiary prevention primary prevention is going to be associated with altering the susceptibility or reducing exposure for susceptible persons right so examples of uh primary prevention is vaccinations or immunizations right uh you're about to go off to college right or I guess you know one a typical 17 18 year old they're about to go off to college and they're going to receive a menitis vaccine right so that's going to be an example of primary level of prevention right or even you're going to go to our health education campaign okay reducing exposure then we have secondary uh prevention and that's going to Encompass like early detection screening and management of the disease right so examples would be cancer screening right or blood pressure monitoring right or a routine mamogram right to detect early stage breast cancer okay but it's screenings and things like that then we have tertiary uh level of prevention and that's going to be uh Rehabilitation providing supportive care reducing the disability and restoring effective functioning right so this is after the disease right um so an example of tertiary level of prevention would be uh stroke therapy to regain motor functions right so physical therapy or we can have a person with diabetes right prescribing them you know insulin for management of their blood sugar levels right or if a person has a heart attack right prescribing some type of drug um to perhaps keep their cholesterol low when we look at homeostasis right whenever we think of physiology right one of the main things you think of is homeostasis right trying to maintain a stable internal environment right um and that's really making sure all of your systems are inbalance right um for homeostasis we're really going to control parameters such as like osmolarity temperature uh pH you know nutrients water you know calcium sugar levels blood pressure things like that right so trying to maintain a you know stable internal environment that's what homeostasis is that's what we trying to you know constantly maintain and Achieve allostasis right is going to be the you know overall process of adaptive change really necessary to maintain survival and well-being so it's your a body's successful ability right to adapt to challenges like I mentioned to maintain survival and well-being right um and Alo stasis you know your adaptation it really is vital for survival during stress now when we look at allostatic overload right so you got to remember this as well allostatic overload is going to be the inadequate adaptation mechanisms or an excessive allostatic load resulting in your inability to maintain homeostasis right maybe you have been you know exposed to multiple stressors back to back to back to back um you're unable to adapt uh to the stressors and then it could lead to um long-term crime IC disease now when we look at the body's you know stress response and when we look at the General Adaptation um response these are the three stages right so you got to remember these three stages okay so the alarm stage right is going to be that first stage that's going to be you know your immediate response right your fight or flight okay right so in the alarm stage right uh you know your fight ORF flight is going to happen right this is where your body is going to uh essentially put some energy in your body right put some energy um for you to in a sense like fight right so in the alarm stage your your heart rate might Spike right you you you might be like in a near Miss accident and your heart rate just goes up right for the resistance stage right this is where your body tries to stabilize and cope with that stress right um you're trying to adjust um to some type of stressor maybe it's like a a demanding job or something like that and you're trying to adjust to that prolonged stress now you're trying to resist um the stress in a sense you're trying to resist you know death really now if you can resist you can stabilize and cope you can bring your body to recovery now if you're not not able to recover you know in that alarm stage you know is persistent right that stress is persistant right this is where we have exhaustion right the breakdown of your compensatory mechanisms right that could lead to um you know permanent failure of systems and even death is possible okay but we have to understand that that General Adaptation response really it helps us to maintain a normal function in spite of the stressor okay so remember all of these stages okay and let's just look at stress right the body's natural stress response and so when that hypothalamus picks up stress it's going to and let's just simply look at this hypothalamic petuary adrenal axis right here right so we already know that the hypothalamus is going to release these hormones in order so the hypothalamus is going to release uh well I don't know why I put H right but the hypothalamus is going to put oh that's why I put H right the hypothalamus is going to release uh CR right critical trop and releasing hormone that's going to go down to the anterior pituitary to release a adrino Tropic hormone that adrino Tropic hormone remember this is our Tropic hormones that's going to go down to the adrenal cortex right so you can release cortisol and cortisol is going to be a type of cortical steroid right it's going to be that stress hormone that we typically talk about right and cortisol is really going to do everything that it possibly can number one to uh prevent hypoglycemia right it's going to stimulate gluconeogenesis as a result right um you have other things happening too really to put some of that sugar into the blood so you can act right in a stressful situation also we have to think about um and stress our sympathetic Pathways as well right so we're going to release for example epinephrine or norepinephrine and you got to also remember what are those effects are going to do to the body right increas in heart rate right um allowing more air to come into your lungs right um dilation of your eyes so allowing more light to enter your eye right so remember the stress responses in general now when we look at some um cell injury right so let me talk about reversible cell injury first right so when we look at reversible cell injury so remember these two different types right so we have hydropic swelling hydropic swelling is the cellular swelling attributed to accumulation of water so water is rushing into your cell why it results from a malfunction of the sodium potassium pump now remember that sodium potassium pump requires ATP right but if there's no ATP it will result in sodium accumulating inside the cell and wherever there sodium water is going to want to follow so water's going to follow and rush into the cell the cell is going to swell up right however it is reversible another type of reversible cell injury is intracellular accumulations and this is where you have the excessive accumulation of substances in the cell right maybe you have too much fat or adapost tissue in the cell okay and also another example of intracellular accumulation is the accumulation of just abnormal substances produced by the cell because of faulty mechanisms or faulty metabolism or synthesis okay so remember that sorry let me go back so when we look at cellular adaptation so you you got to remember these different cellular adaptations as well right so this is like your normal cells right here okay and when we look at atrophy atrophy is a decrease a decrease in cell size right so your cells uh get smaller right and so say for example you're at the gym right you you're you're you're working out constantly right but then you stop going to the gym right so your muscles will get smaller right because uh the stress is not on them as much right when we look at hypertrophy right so hypertrophy is where you have an increase in cell size right so that cell gets larger really due to increased workload on it right so here uh we have like cardiac hypertrophy from like hypertension so you can look at this left ventricle right there look at how large that left ventrical is and I should have put a regular picture of the left ventrical it's not that big and the problem here in that you know left side um uh heart ventricle hypertrophy is look at the Lumen look how small the Lumin is the whole purpose of the heart is to pump blood you're it's not going to pump that much blood when that Lumin is all small right so that's an issue but remember hypertrophy is an increase in cell size whereas hyperplasia right hyperplasia is going to be in increase in cell number right so an example of that would be like the uterine lining thickening uh due to you know hormone or stimulation we have metaplasia so you got to remember this too metaplasia is where we have a conversion of one cell type to another so you're replacing one cell type with another cell type so an example of this would be like we talked about smoking induced replacement of those columnar cells in your Airways with you know squamous cells because squamous cells they're able to um deal with you know the stress uh that that smoking is going to induce right more so than your colonar cells so metaplasia is where you're going to replace one cell type with another when we look at dysplasia right this is that dis ordered growth or the disorderly growth all right these cells look disorganized and whenever you think of displasia think of these as these preo or I'm sorry pre-neoplastic uh cells right these pre pre-neoplastic cells that could turn to be cancerous okay when we look at cell injury right we have necrosis and we have apoptosis right so let me talk about apoptosis first because apoptosis is is you know a normal um physiological process right apoptosis is programmed cell death right so if the cell is no longer needed they're going to it's going to activate uh basically like a self-destruct right um a self-destruct pathway resulting in its regulated underline that regulated cell death right now apoptosis you know we have different Pathways extrinsic or intrinsic Pathways right now I I do mention here the internal pathway right is going to be governed in part by uh p-53 right I won't go so much in depth with it but it's that p53 that kind of ensures that it's basically like a checkpoint so cells won't continuously uh replicate right again apoptosis is programmed cell death necrosis is going to be cell death as a consequence of esea or toxic injury now remember what eske esia is right esmia is just simply um a blockage of blood flow or an interruption of blood flow to an area so a certain area is not getting blood if it's not getting blood it's not getting oxygen right excuse me and when it's too severe it's going to result in cell death right now that cell May rupture you know spilling out its contents into the extracellular fluid as a result the person will feel localized pain um inflammation things like that now I also want you to remember and understand the types of necrosis we have coagulative necrosis remember this is going to be the most common right now this coagulative um necrosis is really going to be due to esmia right we're going to find this type of uh cell death in the heart right we have liquefactive uh necrosis right liquefication of lysosome enzymes and that form Asis or Cy we're typically going to find this in the brain we have fat necrosis right uh death of adapost tissue we're going to find this in the pancreas and you have cous necrosis right you'll find this typically like in the lungs okay neoplasia simply refers to New Growth right more so than likely we now really refer to uh the implication of abnormality of cell growth or a tumor right now when we look at these different terminologies benign growth is generally you know easily curred right whereas malignant neoplasm or neoplasms that's going to be cancer okay so you know benign not as scary right as malignant okay so when we look at the characteristics of benign versus malignant right benign tumors they do not invade adjacent tissue or spread to distant sight meaning they are encapsulated by connective tissue that indicates that is indicative that they are localized right they're not going to invade other tissue or spread these benign growths they're going to grow very slowly they're going to have little vascularity uh they rarely have necrotic areas and they're going to often retain function of that normal origin tissue okay now when it comes to malignant tumors right these are enoplastic tumors with abnormal cell size and abnormal cell shape right these malignant tumors this is what we dislike right they have the potential to kill the host of course if left untreated whereas benign tumors do not these malignant tumors they're going to grow rapidly they may initiate vessel growth right angiogenesis in the tumor and they frequently have necrotic areas and are dysfunctional right I give you an example of like malignant tumor Bronco Broncho carcinoma and so remember these terminologies too right typically we say likea right it's going to be like the banan but when we look at the carcinoma right carcinomas that's going to refer to malignant epithelial uh tumors sarcomas are going to be malignant connective tissue tumors and adenomas will be benign glandular tissue tumors okay now we also got to understand the difference between Proto onogen and anog genes right Proto onogen are simply normal genes that call for normal proteins okay again Proto onogen are normal genes however when we get to enogen these enogen are essentially mutated Proto ancoin causing uncontrolled cell proliferation okay when we look at tumor suppression right these we have tumor suppressor genes right these tumor suppressor genes will cod for tumor suppressor proteins that will stop division of mutated cells so as a result these tumor suppressor genes they basically act like a checkpoint they inhibit cell proliferation keeping most mutations from developing into cancer sorry now I also wanted to talk about um P the p53 gene again right the p53 p-53 gene this is going to be like the most common tumor suppressor Gene right that will inhibit cell cycling now typically we normally have a little bit of p-53 found in your cells it will accumulate um in response to Cellular damage specifically DNA damage right and what p-53 is is is this protein is a transcription factor that binds to damage DNA and regulates a lot of different genes right essentially what it does is it installs cell division allowing time for DNA to repair before DNA replication occurs in that s phas however too much damage uh p-53 will direct the cell to initiate apoptosis right so it's basically a control mechanism right but defects in this p-53 function will disrupt this important quality control system right allowing genetically damaged and unstable cells to survive and continue to replicate right I also want to hit on just lastly chemotherapy right so chemotherapy is going to kill rapidly dividing cells right however we do risk the uh you know infection and imuno supression right we also have tumor markers right and these tumor markers are going to be able to uh these are indicators really used for diagn nois I want to end with grading versus staging okay so you have to understand the difference between grading and staging so grading will refer to the histological characterization of the tumor cells it's basically a determination of the degree of anaplasia right that lack of differentiation right what does it look like now right probably doesn't look like uh that normal cell and the more it doesn't look like that normal cell the uh worse it is right and then we have staging so staging uh refer to the localization or the location I should say and pattern of spread of the tumor right um so how far did it spread right that's what we're looking at staging right um it doesn't involve biochemical testing though of the tumor okay so you got to also remember that okay that's going to be done by cancer grading okay so again understand the difference between grading versus staging okay happy studies