hello and welcome to the emergency care in the streets chapter 9 pathophysiology after you complete this chapter you will have an understanding of cellular changes in response to stressors the understanding of what happens when the cellular system can no longer maintain homeostasis is a key component of patient evaluation and treatment the human body is made up of cells tissues and organs biology is the study of living organisms with regard to their origin growth structure behavior and reproduction pathophysiology is the study of the functioning of an organism in the presence of disease it's derived from greek words meaning pathos is comes from suffering and physicists from form when the condition or functioning of a cellular system breaks down in response to stressors and homeostasis can no longer be maintained disease can grow understanding the cause of the disease process can help in evaluation and treatment to understand how disease may alter cellular function you must understand normal cellular structure and function when exposed to adverse conditions cells undergo a process to attempt to protect themselves from injury change can be permanent or temporary the word atrophy means a decrease in cell size due to a loss of subcellular components it leads to a decrease in the size of the tissue and organ the actual number of cells remains unchanged the decreased size represents an attempt to cope with a new steady state with less than favorable conditions hypertrophy is an increase in the size of the cells due to synthesis of more subcellular components this leads to an increase in tissue and organ size hyperplasia is an increase in the actual number of cells in an organ or tissue usually results in an increase in size of an organ or tissue dysphalesia is an alternation in the size shape and organization of cells most often found in epithelial cells that have undergone irregular atypical changes and then metaphlasia is a reversible cellular adaptation in which one adult cell type is replaced by another human body is composed primarily of water all biochemical reactions occur in an aqueous environment homeostasis can be upset by excessive output or input of fluids such as sweating salt intake or dehydration the average adult takes in about 25 hundred milliliters of water a day or 2.5 liters 60 from drinking another thirty percent from water and foods and the remaining ten percent is a byproduct of cellular metabolism most water is lost in the form of urine which is sixty percent twenty eight percent is lost through the skin and lungs and six percent is lost through feces the degree of fluid imbalance required to compromise homeostasis and cause illness depends on the patient's size age and underlying condition cellular environment changes with aging exercise pregnancy medications disease and injury body fluids can body fluids contain water sodium chloride potassium calcium phosphorus and magnesium plus some other substances the body weight is approximately 50 to 75 percent fluids average male is 60 fluids average female is 50 fluids intracellular fluid is 45 of the body weight an extracellular fluid is 15 of the body weight interstitial fluid is extracellular fluid surrounding tissue cells including cerebral spinal fluid and synovial fluid intravascular fluid is extracellular fluid found within the blood vessels but outside the cells okay let's talk about some disturbances so um first one we're going to talk about is edema and this occurs when excessive fluid builds up in interstitial space you could have peripheral edema and that's in the ankles and feet and is most common form of edema you could have severe edema and it may be caused by long-standing lymphatic obstruction and you could have sacral edema and that may occur in bedridden patients or you could have ascites and that's an abnormal accumulation of fluid in the peritoneal cavity okay and it may be because of several causes so you could have an increased capillary pressure which is from some type of venous obstruction or increased vascular volume you could have pre-menstrual sodium retention pregnancy environmental stress or effects of gravity for prolonged standing okay and then there's decreased osmotic pressure in the capillaries and this is from decreased production of plasma proteins or increased loss of plasma proteins you could also have lymphatic vessel obstruction due to infection or disease of the lymphatic structures or removal of lymph nodes you could also have clinical manufa manifestations and it may be local or generalized you could have pulmonary edema for cardiac reasons or following near drowning incident or overdose when we talk about assessment of edema we want to make sure that we perform an in-depth assessment of including auscultation of breast sounds evaluation for pedal edema and jugular venous distension ekg of course and vital signs and we want to determine a patient's medical history and current and past medications treatment may include diuretics nitrates continuous positive airway pressure which is cpap high flow 2 and advanced airway placement okay so change in water contents can cause a cell to shrink or swell tonicity is the tension exerted on a cell due to water movement across the cell membrane in isotonic solution cells neither shrink nor swell in hypertonic solution water is pulled out of the cells and they shrink in hypotonic solution cells swell isotonic fluid deficit what will happen is you'll have a decrease in extracellular fluid with proportionate losses of sodium and water in an isotonic fluid excess you'll have a proportionate increase in both sodium and water in the extracellular fluid compartment causes of this include kidney and heart and liver failure when dehydration exists orthostatic hypotension so low blood pressure and decreased urine output are common when sodium level is very high hyperthermia delirium and coma may be seen okay so when we talk about sodium the normal serum sodium levels are 136 to 144 okay hyper tonic fluid deficit caused by excess body water loss without a proportionate sodium loss results in hypernatremia which is serum sodium level greater than 145 hypotonic fluid deficit caused by excessive sodium loss with less water loss results in hyponatremia which is serum sodium levels less than 30 135 okay so when we talk about potassium that's necessary for uh neuromuscular control regulation of three types of muscles acid-base balance intracellular enzyme reactions in maintenance of intracellular osmolarity so the normal serum potassium levels are 3.5 to 5. hypokalemia is decreased serum potassium levels and its common cause include decreased potassium intake our potassium shifts into the cells renal potassium losses and extra renal potassium losses frequent complaints include muscular weakness fatigue and muscle cramps the ekg shows decrease and broadening of t waves when you have hyperkalemia this is elevated serum potassium levels it's common causes and cli include there's many causes such as decrease excretion an example is renal failure and shifts of potassium from within the cell such as with burns and excessive intake of potassium this may lead to muscle weakness and flaccid paralysis ekg changes include peaked t waves widening of qrs complex and dysrhythmias and it can be life-threatening calcium administration intravenously immediately antagonizes cardiac conduction abnormalities and bicarbonate insulin and albuterol work in a 15 to 30 minute period okay and then we next we'll talk about calcium and the majority is found in bones and in teeth it provides strength and stability for the collagen and ground substance forming the matrix of the skeletal system it's absorbed from the intestines in a process that depends on the presence of vitamin d so normal serum calcium level is 8.5 to 10.5 when it's low it's called hypocalcemia this is a decrease serum calcium level it can be caused by decreased intake or absorption or increased loss such as with alcoholism endocrine disease and sepsis and symptoms may include spasm of skeletal muscles causing cramps and tenacity laryngeal spasms and seizures when you have too much calcium it's hypercalcemia and this is increase in serum calcium level its cause causes include increased intake or absorption and then such as excess anti um antacid ingestion endocrine disorders and miscellaneous causes so symptoms include constipation or and frequent urination which is polyuria you could have stupid coma and renal failure may develop in severe cases okay so next we're going to talk about phosphate and this is intracellular and on essential too many functions so hypophosphate anemia is a decrease in serum phosphate levels it's caused by decreased supply or absorption excess loss of phosphate such as using diuretics so intracellular shift of phosphate such as after administration of glucose or an extra electrolyte abnormalities and abnormal losses followed by inadequate replication such as diabetic ketoacidosis can cause that okay symptoms include muscle weakness decrease deep tension reflexes and some confusion treatment involves oral replenishment or iv phosphate replacement and then the next one we're going to talk about is high so this is hyper hyperphosphate anemia this is increase in serum phosphate levels it's caused causes include massive loading of phosphate into the extracellular fluid such as excess vitamin d and excretion into the um into the urine such as with renal failure so symptoms may include tremors or paresthesia confusion seizures muscle weakness stupercoma hypotension or heart failure and also a prolonged qt interval the next thing we're going to talk about is magnesium so is the second most abundant intracellular cation it's normal range of serum magnesium is 1.5 to 2.1 hypomagnesia is a decrease in serum magnesium level it's caused by diminished absorption or intake increased renal loss and miscellaneous causes such as diabetes or respiratory alkalosis common symptoms include weakness muscle cramps and tremors treatment causes consists of iv fluids containing some magnesium okay so hyper magnesia is the next thing that's an increased serum magnesium level it results from kidney insufficiency and the inability to excrete the amount of magnesium that you have taken in symptoms include a muscle weakness decreased depth or deep tendon reflexes and confusion okay so when you start talking about disturbances of the acid-base balance understand that acid and bases neutralize each other and must remain in balance acidosis is an increase in extracellular hydrogen ions and alkalosis is a decrease in extracellular hydrogen ions disturbances of acid-base balance are associated with disturbances in potassium balance okay so kidney transport system moves hydrogen and potassium in opposite directions acidosis then is it you excrete hydrogen and reabsorb potassium alkalosis you excrete potassium and reabsorb hydrogen okay so calcium ions also shift in response to the influx of hydrogen a high serum calcium level decreases the rate of of neural transmission a low cerium calcium level leads to hypersensitive neurons and an accelerated rate of neural transmissions okay so types of acid-base disorders so fluctu fluctuations in ph due to bicarbonate levels result in metabolic acidosis or alkalosis fluctuations in ph due to respiratory disorders result in respiratory acidosis or alkalosis when an acid-base disorder is not immediately corrected by the body's buffering system the body initiates compensate compensatory mechanisms patience management often involves treating more than one form of an acid-base imbalance so there are four main clinical presentations of this acid base in balance and the first one we're going to talk about is the respiratory acidosis okay so respiratory acidosis is always related to hypoventilation it's a compensatory mechanism is the renal buffer system and its causes include airway obstruction cardiac arrest overdoses or central nervous system presence near drowning respiratory rest pulmonary edema closed head injury chest injury and carbon monoxide there's a wide range of it reasons hypoventilation can quickly develop a potentially fatal acidosis making it possible for the slow reacting renal system to compensate so what happens are signs and symptoms include systemic or cerebral vasodilation including headaches red flesh skin central nervous system depression braided nausea vomiting and hyperkalemia so chronic obstructive pulmonary disease creates a respiratory acidosis over time gradual destruction of the lung tissue inhibits the exchange of oxygen and carbon dioxide when you have copd so the hypoxic drive is then the only remaining stimulus for breathing so slow onset of this form of respiratory acidosis makes it survivable when you have copd so the second type of acid-base disorders we're going to talk about is respiratory alkalosis and so it's always caused by hyperventilation it's life-threatening events may be responsible for hyperventilation so what happens is carbon dioxide levels drop in the blood forcing a reduction in the circulating carbonic acid so the renal system begins to retain hydrogen ions to to rebalance the shift so then calcium shifts into the intracellular fluid to rebalance the depletion of hydrogen ions the resulting hypocalcemia causes muscle contractions causes of hyperventilation and respiratory alkalosis include drug overdoses especially aspirin some fevers and overzealous back mass ventilations can cause hyperventilation okay so when it comes to respiratory alkalosis signs and symptoms include diminished loss of conscious or level of consciousness lightheadedness carpal pedal spasms tingling lips and face chest tightness confusion vertigo blurred vision hypocalcemia and nausea and vomiting so the third type of acid-base disorder is a metabolic acidosis and then of course the fourth one is metabolic alkalosis so we'll talk about acidosis first and uh it's caused by any acidosis not related to the respiratory system so there could be increased respiratory respirations and a compository mechanism for this condition however um an example would be diabetic ketoacidosis and cushmal respirations which will increase that respiratory rate to try and compensate but um so hydrogen leaks out of the cell and serum potassium shifts into the extracellular space raising the cerium potassium levels calcium also shifts into extracellular space causing hyperkalemia or hypercalcemia which obstructs impulses of neurons in muscles and other tissues yeah causes include when it comes to metabolic acidosis you have cause lactic acidosis caused by cellular respiration anaerobic cellular respiration ketoacidosis caused when cells metabolize fatty acids for energy because they are unable to get used glucose so the byproduct of fat metabolism is ketones it combines or compounds that are extremely acidotic also aspirin overdoses uh aspirin directly stimulates the respiratory center in the brain causing uh tachypnea which leads to respiratory alkalosis so um fast respiratory rate that leads to respiratory alkalosis also alcohol ingestion leading to alcoholic ketoacidosis then you have gastrointestinal loss so signs and symptoms include vasodilation central nervous system depression headaches hot flush skin hypercalcemia tachypnea nausea and vomiting and cardiac dysrhythmias okay and then the next one and final we're going to talk about is the metabolic alkalosis this occurs when there is an excessive loss of acid from increased urine output or decreased acid level in the stomach so common among chronically ill patients causes include upper gi losses of acid such as illness or eating disorders drinking large amounts of water during vigorous exercise or excessive intake of alkaline substances such as antacids compensatory mechanisms in the respiratory system so you could have slow respirations as a means of retaining carbon dioxide increasing the level of circulating acid also signs and symptoms include confusion muscle tremors and cramps and hypotension okay so cellular injury is what we're going to talk about next and it there's various causes hypoxia ischemia chemical injury infectious injury immunological injury so physical damage and inflammation some type of inflammatory injury so manifestations and death depend on how and how many and which types of cells are damaged so it can occur at both a microscopic and functional level so common microscopic abnormalities include cell swelling rupture of cell membranes or nuclear membranes and breakdown of the nuclear material and often results in a change in cell shape and function so functional changes may include an inability to use oxygen appropriately develop of extracellular acidosis accumulation of toxic waste products and an inability to metal metabolize nutrients damage and functional changes in cells often have an impact on the entire organism the entire organ system may fail and dysfunction in one system inevitably affects the other systems repair can occur up to a point with proper treatment so irreversible injuries irreversible injuries will lead to cell death cell death is followed by necrosis and that's a process in which the cell breaks down cell membranes become abnorm abnormally permeable and the cell and its organelle swell okay so the first cell injuries we're going to talk about the cause is this hypoxic injury and it's common cause of cellular injury it's often deadly it may result in decreased amounts of oxygen in the air or loss of hemoglobin function it's a decreased number of red blood cells or disease of the respiratory or cardiovascular system so cells that are hypoxic for more than a few seconds produce mediators that damage other local or distant body locations a positive feedback cycle leads to more cell damage and more hypoxia the earliest and most dangerous mediators are free radicals what free radicals do is they're molecules missing one electron in their outer shell so this results in chemical instability and it causes random attacks on other cells and membranes and it results in widespread and potentially deadly tissue damage so the second type of injury we're going to talk about is a chemical injury and this is common with poisons so cyanide will induce cell hypoxia by blocking um basically the mitochondria and preventing the metabolism of oxygen when it comes to pesticides they block an enzyme present preventing proper transmission of nerve impulses and then also with lead chronic ingestion leads to brain injury and some neurologic dysfunctions it mistaken for calcium in vital biochemical reactions leading to abnormal results and dysfunctions okay and then there's carbon monoxide carbon monoxide binds to hemoglobin it prevents adequate oxygenation to the tissues and this uh causes low levels of oxygen in the body so at low levels though it will cause nausea vomiting and headache higher levels will result in death and then ethanol the lower levels will cause some inebriation but higher doses results in severe central nervous system depression hypoventilation and cardiovascular collapse and then pharmacologic agents produce toxic products when metabolized in the body especially in overdose conditions so that's the chemical injuries okay so the next uh injury we're going to talk about is the infectious injury and infectious injuries to cells occur as a result of an invasion of bacteria fungi or viruses so bacteria can cause injury by a direct action on the cells or the production of toxins that causes the injury the viruses can initiate an inflammatory response this leads to cell damage and the symptoms that you're going to see in the patient then you have brilliance that's measures the disease causing ability of the microorganism and the pathogenicity is the function of the organism's ability to reproduce and cause disease within the human body growth and survival of bacteria in the body depend on the effectiveness of the body's own defense mechanisms the bacteria's ability to resist those mechanisms so newborn infants older adults and people with diabetes and people with cancer or other chronic diseases tend to have weaker immune systems so let's get a little bit more in depth and break them down so first one we're going to break down is bacteria and many possess a capsule that protects them from ingestion or and destruction so phagocytes are cells that engulf and consume for materials so categorize depending on the results of gram staining gram staining is a suspension of bacteria is stained with a purple dye and then an iodine solution so um then discolorized with alcohol and other solvent then stain with red dye so bacteria that resist discoloration are called gram-positive bacteria bacteria that accept the color stain are called gram-negative bacteria and so what happens are they produce exotins or endotem toxins sorry exotoxins or endotoxins that can injure or destroy cells so exotoxins are produced within the cell and released into surrounding tissues or fluids they're poisonous they actions vary inactive exotoxins are sometimes used for vaccines then you have endotoxins and they are lipo polysaccharides that are part of the cell walls of gram-negative bacteria so they cause inflammation fever chills and malaise they may cause septic shock if present in large amounts and they re remain active even after the bacteria is destroyed this is the body's most common reaction to the presence of bacteria is inflammation and then we need to talk about viruses so intracellular parasites that take over uh the metabolic process of the host cell and use the cell to help them replicate they consist of nucleic acid core of either rna or dna and capsaice is a layer of protein that protects the virus from phagocytosis so replication occurs inside the host cell a symbolic relationship symbionic relationship between the virus and the normal cells may be the cause of a persistent unapparent infection the next one we're going to talk about is the immunologic and inflamma inflammatory injury so inflammation is a protective response that can occur with even without bacterial invasions so you could have an infection it's characterized by an invasion of microorganisms that cause cell or tissue injury leading to an inflammatory response and it can be triggered by an agent that is physical chemical or micro biologic so local effects include dilation or expansion of the blood vessels and increase vascular permeability okay so signs include heat redness tenderness swelling and pain and then of course the outcome depends on the amount of tissue that's damaged so you could have a mild inflammation that results in a return to normal tissue or more severe inflammation results in destroyed tissues that must be repaired so you could have scar tissue replaces large areas of tissue destruction okay so now the next injury factor that we're going to talk about is the genetic factor and so genetic factors that may damage cells include chromosomal disorders or premature developmental development of atherosclerosis or obesity sometimes and then you have an abnormal genes may develop and if a gene mutates during meiosis it can affect newly formed fetuses by hereditary you can have genetic factors that cause injuries or due to some other later cause in life so examples of diseases with genetic link include down syndrome and rheumatoid arthritis okay and then you have injuries which are related to nutritional imbalances and so um of course good nutrition is required to maintain good health and assist the cells in fighting off diseases but injurious nutritional imbalances include obesity or malnutrition or some type of vitamin or vitamin access or excess or deficiency or mineral excess or deficiency these conditions can lead to alterations in physical growth mental and intellectual retardation and death and then you have physical agents or conditions that can cause injuries and so these include heat cold or radiation and they may cause injury by burns frostbite radiation sickness and tumors the degree of the cell injury is determined by this the strength of the agent and then the length of the exposure okay so the next injury we're going to talk about is apoptosis and this is basically normal cell death and so basically cells are genetically programmed and as part of the normal development uh immune function and tissue grows the cells exhibit characteristics of nuclear changes and dye in well-defined clusters and so what happens is it's a basically activation of genes that are encoded for proteins known as capsasis eventually leads to cell suicide it's controlled degradation allows their remnants to be taken up and reused by neighboring cells but it can be prematurely activated by pathologic factors such as cell injuries some forms of heart failure can result in early cell death death of liver cells in patients with viral hepatitis you could see this happen and the inhibition of normal function allows destructive cellular proliferation so such as with cancer or rheumatoid arthritis you can see that occur and then the last injury we're going to talk about is abnormal cell death and necrosis that results of the changes that occur following cell death and living tissue so you have simple necrosis and basically areas of necrosis where the gross or microscopic tissue and some of the cells are recognizable and it may be caused by acute ischemia acute toxicity or a direct physical injury and then you have derived necrosis the causation necrosis manifested by the loss of all features of tissue and cells so you could have some dry gain green that results from invasion or precipitation of necrotic tissue after the blood supply is compromised fat necrosis and that results from the destruction of fat cells usually by enzymes and then liquefication necrosis and that results from coagulation necrosis followed by conversion of tissue into a liquid form and invasion of putrifying bacteria okay so the next area we're going to talk about with the pathophysiology is going to be hypoperfusion now hyperperfusion is the major major thing that you're going to be dealing with when it comes to paramedic or pre-hospital medicine and so perfusion is the delivery of oxygen and nutrients and removal of waste from cells organs and tissues by the circulatory system so hypoperfusion occurs when the level of tissue perfusion decreases below the below normal okay okay so when the body senses tissue hypoperfusion it will set compensatory mechanisms into motion and sometimes this is uh sufficient to stabilize the patient other times it overwhelms that normal compensatory mechanism and the patient's condition deteriorates when the patient's condition deteriorates it's considered dead compensate decompensated shock and when the body's able to compensate it is called compensated shock easy enough right okay so we're going to talk a little bit about the body's response to hypoperfusion next the body releases catecholamines and those catecholamines are epi and norepi and that will produce vasoconstriction so the norepi and the epi will produce vasoconstriction the a-r-a-a-s is activated in an antidiuretic hormone is released from the pituitary gland this action triggers salt and water retention as well as peripheral vasoconstriction and what that does is it's trying to increase blood pressure and cardiac output at that time fluid will shift from the interstitial tissues into the vascular compartment the overall response is to increase the preload stroke volume and heart rate so that the blood volume is adequate the result is often an increase in cardiac output and myocardial oxygen demand persistence results in a continued increase in myocardial oxygen demand okay and so the compensatory mechanisms can no longer keep up with the demand and myocardial function will worsen tissue perfusion will decrease causing impaired cell cellular metabolism and fluid may leak from the blood vessels causing system systemic and pulmonary edema okay so other signs may be dipsnia or a dusky skin you could have low blood pressure or impairmentation so the next thing we're going to talk about is shock when it comes to paramedic of we just talked about hypoperfusion you have to talk about shock next uh they are very interrelated so shock is an abnormal state associated with inadequate oxygen and nutrient delivery to metabolic apparatus of the cell this will result in in paracel metabolism and inadequate perfusion of vital organs remember if the cell isn't getting oxygen or the body's not getting oxygen the cells are going to revert to this anaerobic metabolism and what's going to happen is it's going to cause an increase in lactic acid production and metabolic acidosis decrease oxygen for the hemoglobin decrease atp production and changes in electrolytes cellular edema and release of enzymes glucose impairment leads to elevated blood glucose levels due to re release of catecholamines and cortisol okay and um when it when you are talking about shock it can occur due to the inadequacy of a central circulation or of a peripheral circulation okay and so this occurs basically when you have central shock it's um consists of cardiogenic shock and obstructive shock when you have peripheral shock it includes hypovolemic shock and distributive shock now we're going to break those down in more detail next and we're going to start with the central shock and when you think of central shock i always think of the the harder the lungs in the central area of the body and so cardiogenic shock is the first one we're going to talk about and this occurs when the heart cannot circulate enough blood to maintain adequate peripheral oxygen delivery so most common cause is a heart attack and mi so mitocardial infarct is the most common cause of cardiogenic shock obstructive shock occurs when blood flow becomes blocked in the heart or great vessels so remember both types of central shock cardiogenic and obstructive are obstructive think about there's some type of obstruction causing the inadequate blood flow so what could cause obstructions in um in the central area so we have pericardial tamponade and remember pericardial tamponade is basically when there's fluid in that pericardial sac surrounding the heart so the heart can't fill or pump because there's that pressure on that pericardial sac also another form of obstructive shock is the aortic distent or aortic dissection so of course uh loss of blood flow because the aorta is dissecting you have left atrial tumor which could obstruct flow between the atrium and ventricle in it so there's some type of tumor in that area you also have obstruction of either superior inferior vena cava that's going to decrease that cardiac output of course and a large pulmonary emboli or a tension pneumo it may prevent adequate blood flow to the lungs okay so that's that obstructive shock which is the central type of shock and then you talk about peripheral so that's the second one so central or peripheral peripheral i always think of the peripheral extremities or the outlying areas so um when it comes to peripheral shock you could have hypovolemic shock okay so hypovolemic shock it's um when the circulating blood volume is unable to deliver adequate oxygen and nutrients to the body and there's two types of the of this hypovolemic shock okay and we're going to talk about those next okay so the two types are exogenous or endogenous and it depends on where the fluid loss is occurring external bleeding is the most common type of exogenous hypovolemic shock an endogenous shock occurs when the fluid loss is contained within the body that was hypoblaming shock and now we're going to talk about the second type of peripheral shock and it's distributive shock and so distributive shock occurs when there is a widespread dilation of the vessels and so when you have circulating blood volume pulling in an expanded vascular bed the tissue perfusion decreases okay you know let's go back to this slide and the most three common types we're going to talk about of the distributive shock are anaphylactic shock and that's anaphylaxis and basically histamine and other vasodilatory proteins are released upon exposure to an um an allergen accompanied by wheezing in near dicario this results in widespread vasodilation it causes fluid to leak out of the blood vessels and into the interstitial spaces the second type of distributive shock which is peripheral shock is septic shock and this is a widespread um basically results in a widespread uh from a widespread infection if normal immune mechanisms become overwhelmed the body produces a multitude of substances that cause vasodilation this decreases cardiac output if untreated it will result in multi-organ dysfunction syndrome and death then the third type of um distributive shock is going to be also peripheral shock so um that's neurogenic shock and it usually results months from some type of spinal cord injury and the loss of normal sympathetic nervous system tone and vasodilation is lost and so you just see a widespread dilation of that vessels so now we're going to talk about management now that we know what the uh hypo perfusion is and shock now we're going to talk about management of it so most types of shock are characterized by reduced cardiac output cardiac insufficiency and a rapid heartbeat okay and so determining the presence or absence of shock requires the evaluation of the presence and volume of the peripheral pulses in absence of an organ perfusion and function so the strength of the peripheral pulses is related to both stroke volume in the heart and the pulse pressures normal skin perfusion results in being pink warm and dry right and so shock it will result in a slow delayed or prolonged capillary refill capillary refill to test briefly squeeze the toenail or fingernail and look for the return of color normal refill time is less than two seconds right but modeling polar peripheral essential cyanosis and delay cap refill may signal the presence of shock accuracy of cap refill is measured measurement decreases after the age of six however so not as useful in adult population because of the redu reduction in peripheral circulation but when we talk about management of shock measuring in tidal carbon dioxide or etco2 may also be useful you can interpret the effectiveness of perfusion using end tidal co2 decreasing levels of end tidal co2 are an early indicator of shock and low levels of etco2 combined with other signs and symptoms are omnious clinical findings the next thing we're going to talk about is multiple organ dysfunction syndrome or mods mods is a progressive condition that occurs in some critically ill patients it's characterized by concurrent failure of two or more organs or organ systems that are initially unharmed so you have types of mods so you have a primary mods or you have a secondary mod so primary mods results uh direct results of an insult or secondary mods it's a slower more progressive organ dysfunction okay and when you talk about pathophysiology you have to talk about the body's defense mechanisms and these are the self-defense mechanisms so the immune system includes all structures and processes associated with the body's defense against foreign substances and disease-causing agents now you have three lines of defense you have the um anatomic barriers you have the immune responses and then you have the inflammatory responses when you talk about the anatomic barriers basically there are several that decrease the chances of the body being invaded by forward substances and these are the skin you have the hairs in the upper respiratory tract in the lining of the lower respiratory tract and then you have acid in the stomach when it comes to the immune response now this is the body's defense reaction to any substance that is recognized as foreign it's directed towards invading microbes which are bacteria viruses also triggered by foreign bodies and even abnormal growths in cells okay so cellular interactions in the immune system so it depends on the particular challenge but the basic pattern is the same bacteria will enter the body and if they are not encapsulated macrophages begin to ingest them okay so if they are encapsulated though antibiotic antibodies coat the capsule so they can be ingested by phagocytes components of the cell wall activate the complement system okay so basically already existing antibodies will assist by acting as neutralizing the bacterial toxin memory b cells attract to the infected sites will be activated if they encounter an antigen they recognize if infection is new to the body b cells will then be activated okay so on this slide you're going to see the immune response system cells you could take a look at that that's on table 9-5 in your book okay so when you comes to immune responses you have two different types you have a natural or native and and then you have an acquired immunity and they both protect the body from infectious agents and form substances so the natural or native immunity that uh that is non-specific cellular um or a humeral response that operates as a first line of defense against the pathogens it's associated with the initial inflammatory response and then you have an acquired or adaptive immunity that's a high specific method in which the cells respond to an immune stimulant with this acquired immunity now that is passively acquired in its performed antibodies and not usually from mother to infant that acquired immunity it comes to this immune response it's really important the paramedics understand this understand that you're gonna have this primary or initial immune response and that takes place during the first exposure to an antigen an antigen is otherwise known as some type of foreign substance that the body notices or or thinks then you have a secondary immune response and that occurs to on repeat exposure to that foreign substance okay so let's break this down a little bit further and the beginning or the induction phase of an immune response occurs when immune system recognizes an antigen so an antigen may be immunologic or immunogenic which is not it will have a some type of response or a non-immunogenic which does not elicit a response you have antibodies and that binds a specific antigen so that the complex can attach itself to a specialized immune cell and destroy the complex or induce a response so you can see it in this um slide right here you can see that the antigen the antibody are going to combine to form that antigen antibody complex all right so an immunogen is an antigen capable of generating an immune response against itself a haptin is a substance that normally does not stimulate an immune response but that can be combined with an antigen at a later time to initiate a specific antibody response on its own okay so we're going to talk about the humoral immunity and b cell lymphocytes produce antibodies or immunoglobulins that react with a specific antigen when it comes to the humoral immune response okay so b lymphocytes are born in the bone marrow and basically in stem cells okay and so what happens for b cells to produce antibodies they must be activated and the most common way that this occurs is via helper t cells microphanges engulf the antigen via phagocytosis and it pushes discarded particles into the cell surface where they interact with b cells and a helper t cell antigen binds with the b cell and the helper t cell activating both helper t cells secrete a lymphos lymphocyme which stimulates b cell to produce a clone clone has two identical cells that have two different functions you have the plasma cells which make antibodies and then you have the memory cells and the they remember the encounter with that antigen okay so this is a really good slide of what we just talked about you could see the beginning you could see that microphage phage engulfing the antigen with phagocytosis and then you see discarded materials being pushed and they interact with b cells in that helper t cell okay then you see um those helper t cells secreting that uh lymphocyme which stimulates the b cell to produce the clone just as i said right and then you see that memory cell in the cell mediated immunity the activation often occurs via those helper t cells which we talked about earlier and and then that clone that antigen binds to the b cell and helper t cell and then just as we talked about it produces that clone all right so we're going to talk about immunoglobulins and they are antibodies secreted by the b cells they consist of crystallized fragments um and two antigen binding of fragment regions so they bind only to a specific antigen and you could see that also in the photo right there and basically the basic antibody molecule has four chains linked into a y shaped and each side of that identical is identical with one light chain attached to a heavy chain okay so there are three main categories of antigens and antibodies there's the isotopic antigen marker and it occurs in all members of a subclass of an immunoglobulin class then you have the allotypic and that antigen marker is found on some members of a subclass okay and then you have the idiotic and that is a determinant is unique structure created on the light and heavy chain of the immunoglobulin molecule all right so we're going to talk about antibodies they make antigens more visible to the immune system in three ways all right and so they make them more visible by um opsinization and this is an antibody coats an antigen to facilitate its recognition by the immune cells and antibodies cause antigens to clump for easier phagocytosis and then antibodies bind to and inactivate some toxins produced by bacteria so micro fanges can ingest them okay and then you could see the general classes of those immunoglobulins on the chart on 9-6 okay so next we're going to talk about cell mediated immune responses so cell mediated immunity is characterized by the formation of a population of lymphocytes that can attack and destroy foreign material they're the main defense against viruses fungi parasites and some bacteria okay so the mechanisms by which the body recognizes transplanted organs and eliminates abnormal cells that sometimes arise all right so the t-cell lymphocytes recognize antigens and contribute to the immune response in two ways they secrete uh cytokines that attract other cells and become cytotoxic and kill infected or abnormal cells so there are five subcategories of t cells and we're going to talk about those next so you have the killer t cells and they destroy antigens you have helper t cells they activate immune cells including b cells and other t cells you have suppressor t cells and those suppress the activity of other lymphocytes so they can or they do not destroy normal tissue you have memory tissue cells remember the reaction for the next time it is needed is what those memory t cells do and then you have this lymphocene producing cells they work to damage or destroy cells infected with a virus okay so an inflammatory response is the response of a body of the body to irritation or injury it's characterized by pain swelling redness and heat and the most common causes are injury and illness infection and injury right so you have the acute inflammation and this involves both vascular and cellular components it's um basically it causes blood vessels to expand vessel wall becomes thinner and fluid leaks into that interstitial space and this causes edema and when enough pressure has been released vessel walls contracts and outflow slows this leads to stasis of blood in those capillaries with the acute inflammation you have a variety of cells participating you have white blood cells which are the leukocytes platelets mast cells plasma cells which are the b lymphocytes and then specific cell types include neutrophils monocytes lymphocytes basal basal fills and activated platelets so chemical mediators account for the vascular and cellular events that occur this includes histamine and then some type of acid derivatives and cytokines mast cells degranulate and release a variety of substance the major stimuli for d granulation are physical injury chemical agents and immunological substances they release a vasoactive and and mines and histamine and serotonin it increases vascular permeability uh it causes vasodilation and can cause bronchial constriction nausea and vomiting they synthesize leukotrienes which is a slow reacting substance of anaphylaxis okay and then they simply synthesize pros dana glanins next part or next inflammatory response we're going to talk about is the plasma protein system and this is plasma derived mediators that modi modulate the inflammation inflammatory response it's a complement system basically and it's a group of plasma proteins that attract white blood cells to site sites of inflammation activate white blood cells and directly destroy cells so the components are basically you have the c3 it's a central compound it's produced by one of the two pathways a classic pathway it starts when the antigen and antibody complex combines to the um complement all right and so they activate um indep is dependent on the process of these antibodies okay and then you have the second one is an alternate pathway it's triggered by a bacterial toxin and does not need antibodies to be activated okay so the next inflammatory response we're going to talk about is the plasma protein systems and that is the coagulation system and it performs a vital role in the formation of blood clots and facilitates repairs of that vascular tree so inflammation triggers a series of reactions that encourage fibrin formation and fibrin is a protein that basically bonds to form fibrous component of the blood clot and the um what happens is there's a cascade it activates to dissolve the fibrin and create fibrin split products all right and then the pros of a protein system we're going to talk about is going to be the uh kinin system and this leads to the formation of a vaso active protein bradykinin from a calicrine and so the uh calicrine enzyme normally found in the blood plasma urine and body tissue is in the inactive state and basically um it activates and it increases vascular permeability dilates blood vessels contracts smooth muscle and causes pain when injected into the skin and you have the hagam man factor and that spurs the kidney system into action so this triggers intrinsic clotting cascade which occurs when blood is exposed to collagen and other substances so the cellular components of inflammation so the goal is for inflammatory cells specifically these neutrophils to arrive at the sites within tissues where they are needed the there's two major stages and so you have the intravascular phase and that's when leukocytes move to the sides of the blood vessels and attach to the specific cells and then you have extravascular phase and that's when leukocytes travel to the site of the inflammation and kill the organisms and what happens you have this cellular event response okay you have the marginalization and that's a loss of fluid cause causes blood to increase its viscosity so blood flow slows and produces stasis leukocytes move towards the sides of the blood vessels and bind to epithelial endothelial cells the activation the mediators trigger the appearance of basically um integrins on the surface of these epithelial cells and you have adhesion so the they actually attach to those uh endothelial cells you have um a permanent permeation through the vessel wall moving to that interestial space okay and then these pm pmns move towards the site of the inflammation in response to that uh chemotactic inflammation process and it basically on this slide it's going to show you that cut cellular component in in that shifting of the moving to the vessels moving out of the vessels moving to the sites that's showing you that process next we're going to talk about the cytokines and they they're products of cells that affect the function of other cells and so when you talk about this you have those interleukins they attract white blood cells to the sites of the injury and then you have the interferon and that is proteins produced by cells invaded by viruses so they are released into the bloodstream or intracellular fluid to induce healthy cells to manufacture an enzyme that counters the infection and so those are the two type of cytokines okay so lympha kind stimulates leukocytes and a microphages activating factor stimulates microphages to engulf and destroy foreign substances there's a migration factor that keeps white blood cells at the site of the infection or injury until they can perform their designated task okay so injury resolution and repair when it comes to that normal wound healing involves four steps you have a repair of the damaged tissue you have rep removal of the inflammatory debris restoration of the tissue to the normal state and then regeneration of cells when it comes to healing after an injury or loss depends on the type of cells that make up the affected organ okay so you have um the label cells and they divide continuously so organs derived from these cells heal completely then you have stable cells and they are replaced by regeneration from remaining cells and then you have permanent cells and they cannot be replaced scar tissue is laid down instead so wounds can heal by primary intention and this occurs in clean wounds with opposed margins and then you have secondary intention and this occurs in large gaping or infected wounds it's more pronounced and prolonged inflammatory response so you have factors that lead to dysfunctional wound healing and it may be local or systemic and so when you have these you so systemic factors include poor nutritional intake or hemologic abnormalities so diabetes and aids affects the cells of the immune system increasing the chance for infections and corticosteroids suppress the initial inflammatory response required for the proper formation of scar tissue and increase the risk of wound infection wound separation slows down and the healing process as healing needs to start over to some extent all right so chronic inflamma inflammatory responses and um these causes include a successful acute inflammatory response to a foreign body or a persistent infection or persistence or presence of an antigen it's associated with an infiltrate or pus containing monocytes and lymphocytes it's usually involved tissue destruction and repair events are similar to those in acute inflammation process but also include the growth of new blood vessels okay so we're going to talk about variances in the immunity and inflammation next and so hypersensitivity is any response of the body to any substance to which a patient has increased sensitivity you could have an allergy and that's hypersensitivity reaction to the presence of an antigen or otherwise known as an allergen you could have an autoimmunity and that's produced or production of antibodies or t cells that work against the tissue of its own body and then you have osmond immunity iso immunity and that's formation of t cells and or antigens or antibodies directed against the antigen on another person's cells and that's typically um after organ transplant or some type of blood transfusion and so let's talk about type one so type one is an immediate hypersensitive or hypersensitivity reaction and it's acute reaction to that stimulus okay and so basically the reaction may be immediate um and uh it's uh involves interaction between the stimulus and a performed antibody of the ige type severity of the symptoms depend on the extent of the mediator response and it varies from life-threatening to maybe to a mild basically milder reaction and then so this is type one and uh treatment in the field includes administrations of epi via epipen auto injector or some type of subcutaneous injection of ep you have type 2 and basically this is the um cytotoxic hypersensitivity this involves a combination of that ig or igm antibodies with antigens on that cell membrane remember we talked about that earlier cells are destroyed by this fixation or by another antibody so that healthy cells may be destroyed it occurs within a few hours of the exposure examples include blood transfusions so when you think about the blood transfusion or that reaction to it this is a type 2 type 3 you have tissue injury caused by immune complexes so it occurs within a few hours of the exposure reactions may be systemic or localized systemic form is results from a large single exposure to an antigen and then a localized is consistent of a basically an area of vascular inflammation and then next moving on the last but not least we have type 4 that's a delayed or cell mediated hypersensitivity it's primarily mediated by some soluble molecules that are released by specifically activating t cells you have also two subtypes you have a delayed and then you have that cell mediated type moving on we're going to move into the targets of hypersensitivity reactions so you have allergic reactions and this is caused by or target is an antigen or an allergen you have an autoimmune reaction and this is targets is the target is a person's own tissue and so when you talk about autoimmune reactions specifically we could break it down into even further you could talk about graves disease and that's an autoimmune disease that's caused by thyroid stimulating or thyroid growth immunoglobulins and then you have type 1 diabetes mellitus that's um some agent causes the body to produce antibodies or auto antibodies against beta cells okay so that's type 1 diabetes you have rheumatoid arthritis and that's a chronic systemic disease it's one of the most common forms of forms and it's characterized by inflammation of the synovium and the synovium is a connective tissue membrane lining the joints okay so that's rheumatoid arthritis that's a chronic most common um type of an autoimmune disease next one we're going to talk about an autoimmune reaction is the myosthenia gravis and that's an acquired autoimmune disease and that's characterized by attack on the nervous muscle junction the next one is neutropenia and that's a decrease in the circulation of neutrophils and it decreases the body's ability to fight reactions okay so itp is a blood disorder in which the patient forms antibodies two blood platelets that cause their destruction so bleeding is the main symptom treatment is based on the severity of symptoms and the platelet count then you have systemic lupus and that's the body's own immune system is directed against the body's own tissues you know deficiency is an abnormal condition in which some part of the body body's immune system is inadequate you have congenital immunodeficiencies and they those are defects which involve the lymph node stem cells and affects both t and b um cells okay so then you have the x-linked um and that affects male infants and it's caused by a defect in uh the differentiation of the pre-b cells and the b cells okay so that affects those the male vince and then you have isolated deficiency of iga and that results from a block in the terminal differentiation of the b lymphocytes okay so you could have acquired immunodeficiencies when you talk about acquired emission immunodeficiencies the contributors to this condition include new nutritional deficiency stress trauma hypoperfusion or shock you have mediator production damage to vital organs or decreased nutrition occurring during trauma states you also have the um immunodeficiency basically it's the most frequently caused by drugs so that's treatment induced and it's often a therapeutic benefit however it may lead to other types of diseases so physicians are usually cautious about prescribing this therapy for long periods of time for a long time physical or mental stress has been shown to decrease white blood cell and glucose leukocyte function so and then aids is caused by an rna retrovirus hiv which binds to helper t cells infecting and killing them replacement therapy for some types is how you um you would treatment of immunodeficiencies and so you could they have intravenous gob gamma globulin and that's used in therapy of a number of immunologic disorders of the nervous system also bone marrow transplants and this is used in persons with acquired causes of the immunity deficiencies and then transfusions are also used as treatment of immunodeficiencies there are factors that cause diseases and these factors are genetic environmental age related and sex associated factors can cause or contribute to diseases genetic factors are present at birth and are passed through a person's genes to future generations environmental factors include microorganisms immunologic and toxic exposures personal habits and life styles exposures to chemicals and physical environment and psychosocial and environment so uh the autoatomic causes include um the male rotation of the colon degenerated diseases of the spine or a aortic stenosis and immunological reaction may result in disease also have an agent that triggers an abnormal response against melon and this is the it leads to the development of multiple sclerosis so you have uncontrollable and controllable factors that cause diseases uncontrollables of course are factors that include genetics and race then you have controllable factors which are smoking drinking alcohol inadequate nutrition lack of physical activity and stress now you have age-related risks and risk of a particular disease often depends on the patient's age so newborns are at risk because immune systems are not fully developed and teenagers are at risk because of trauma use of drugs and alcohol older adults older adults greater risk for cancer heart disease stroke and alzheimer's disease okay then you have sex associated factors and uh and these include um prevalence more in one sex than the other and so some diseases are more prevalent in men than in women and vice versa so more prevalent in men is lung cancer gout and parkinson's disease more prema prevalent in women are osteoporosis rheumatoid arthritis and breast cancer and presentation of the disease can differ from men to women as well when you start to analyze the disease risk there are conversational risk factors and those are factors that can directly cause a disease to develop and then there's non-causational risk factors and those are factors that are associated with the risk for the disease but not a direct cause all studies should consider the incidence prevalence morbidity and mortality of the disease and incidence is the number of new cases in that population prevalence is the number of new cases in a particular population within a particular period morbidity is the presence of disease or incidence or prevalence of the disease and then mortality is the number of deaths from the disease in a given population expressed as a proportion okay you could look at the slide and you could see the risk factors um often interact and this is a showing common respiratory diseases it's on table 9-11 chapter 9. all right and then you have common familial diseases and so when it comes to common common familial diseases and associated risk factors you have a genetic risk and that's one that is passed through generations by inheritance inheritance of a gene you have a familial tendency and that's cluster of diseases in a family group despite lack of evidence for heritable gene associated abnormalities then you have an autosymmonial dependent or dominant that's a person needs to inherit only one copy of a particular form of the gene to show that trait and then you have an immunologic disorder and it's caused by either hyperactivity or hypoactivity of an immune system okay most that exhibit familial tendencies involve an overactive immune system when it comes to allergies they're acquired following an initial exposure then you have asthma it's a chronic inflammation condition of course and then this is just showing common familial diseases uh a chart and the reaction of that and then we talk about cancer this includes a large number of malignant growths uh prognosis often depends on the extent of the spread so the spread is metastasis metastasis and the effectiveness of the treatment so lung cancer is the leading cause of death due to cancer in the united states major risk factors is cigarette smoking eight alterations in genetic material lung cancer that may suggest a genetic tendency other predisposing factors include exposure to asbestos coal products and other industrial chemical products symptoms include cough difficulty breathing blood tinge sputum sputum and repeated infections and then you have breast cancer the most common type of cancer in women women who first degree relatives have breast cancer are two point times 2.1 times more likely to develop the disease risk factors are they vary with age at which the affected relative was diagnosed five to ten percent of patients have a pattern of autosomal de dominant inheritance and then a colorectal cancer it's the third most common type of cancer in both males and females relatives of patients with colorectal cancer are more likely to have the disease themselves symptoms may be minimal such as small amounts of blood in the stool and treatment involves surgery and sometimes chemotherapy endocrine disorders so diabetes mellitus is a chronic disorder of the metabolism associated with either partial insulin secretion or total lack of insulin secretion by the pancreas symptoms includes excessive thirst and urination weight abnormalities and the presence of excessive glucose in the urine and blood ketoacidosis comes with type 1 diabetes and that is insulin dependent diabetes mellitus non-ketoacidosis prone that's type 2 diabetes that's non-insulin dependent diabetes hemophilia when you talk about hemophilia hemophilia and anemia that's characterized by increased destruction of red blood cells there's a number of causes rh factor blood transfusion reaction uh disorder is of the immune system and then you have the hemophilia um which is the basically there's an inherited disorder which is characterized by excessive bleeding that's sex link condition and it occurs only in males passed from the mother to the sun hemoglobin that's when the body absorbs more iron than needed excess iron is stored in various organs it can lead to diabetes heart disease liver disease impotence and a bronze skin color and this shows that disease on the slide so dietary iron it shows confined with the protein and you could go through that the slide and then common passed down familial diseases you could have cardiovascular disorders and which range from long qt syndrome it's a cardiac condition system abnormality resulting in a prolonged prolongation of that qt interval on the um on the ecg and so it's considered a life threat if you have an extra exercise induced syncope or syncope associated with chest pain or history of syncope or syncope associated with um startle okay so cardi and the next cardiovascular disorder we're going to talk about is cardiomyopathy and that's a disease of the myocardium it leads to heart failure acute mis and death mitral valve prolapse that's a mitral valve leaflet balloons into the left atrium during systole you could have cardio or coronary heart disease it's called by impaired circulation of the heart and then high blood pressure or hypertension also some types of renal diseases are are passed down from generation to generation including gout that's an abnormal accumulation of uric acid due to a defect in the metabolism what happens it is accumulates in the blood and joints it causes pain and swelling more common among men than women and usually has a genetic basis if left untreated it causes destructive tissue changes in the joints and kidneys and treatment includes diet and drugs also kidney stones those are small masses of uric acid or calcium salts that form in any part of the urinary system often causes severe pain nausea vomiting when the body attempts to pass them researchers have found a gene that causes the intestines to absorb too much calcium and uric acid stones often have a genetic basis gastrointestinal disorders are known to be passed down so peptic ulcer disease and basically that's erosions in the lining of the gastrointestinal tract gallstones are stone-like masses in the gallbladder obesity is an unhealthy accumulation of body fat morbid obesity of course is more than or greater than a body mass index of 40 kilograms and overweight that's a bmi of 25 to 29.9 and then a neuromuscular disorder so huntington's disease that's characterized by progressive um basically cornea and mental deterioration muscular dystrophy that's acute that's a group of hereditary diseases of the muscular system multiple sclerosis that's when the millennium melanin sheath surrounding the nerve fibers of the brain and spinal cord become damaged also alzheimer's disease that is a common of familial disease passed down and it results in atrophy loss of neurons in ventricular enlargement in the brain and then schizophrenia is a psychiatric disorder which is passed down it's a group of mental disorders distortions of reality withdrawal and disturbances of thought language perception and emotional response and bipolar disorder is a common familial disease it's characterized by episodes of mania and depression all right so when we start talking about stress and disease stress is the medical term for a wide range of strong external stimulus that causes a physiologic response okay so um basically the physiologic stress um is a change that makes it necessary for cells of the body to adapt so there's three concepts of that and it includes the stressor the effects and the body's response to that usually response to stress is appropriate and beneficial however unchecked stress response can result in outcomes which are detrimental including chemical dependency heart attacks stroke depression headaches and abdominal pains okay so you have a general adaptation syndrome and you have different stages it's characterized by three stages of reaction to stressors when you have the first stage that's the alarm and a body reacts to by releasing catecholamines such as uh epinephrine which is adrenaline and norepi which is nora adrenaline and dopamine so adrenaline of course we know this acts as a neurotransmitter and cns and as a hormone in the blood okay and so um basically norepi is a primarily a neurotransmitter of the peripheral sympathetic nervous system and so effects are going to include increased respiratory rate decreased blood flow to the skin smooth muscle constriction and various effects on the liver that increase the body's ability to lose glucose this is basically that fight or flight response and it can either prepare the body to deal with stress or it could weaken the immune systems and then you have type 2 or stage 2 that's the body's way of adapting to stressors it stimulates the adrenal gland to secrete two types of corticosteroid hormones that increase blood glucose levels and maintain blood pressure all right so the hypothymus stimulates the anterior pituitary gland to release acth and that targets adrenal cortex to release cortisol what it does is it stimulates cells to increase energy production and increases serum glucose levels and impairs the use of glucose by peripheral tissues when it comes to and just what we just said is is on this slide so um that act is stimulated other hormones are released and um so this reduces inflammation when it served its purpose it increases red blood cell production and affects electrolyte levels it decreases the size of lymphatic tissue which plays a role in immunity and other hormones related to stress okay and then the third stage we have is exhaustion so exhaustion adrenal glands become depleted diminishing the level of blood glucose and that results in decreased stress tolerance progress or progressive mental and physical exhaustion illness and basically collapse so the body's immune system is compromised and reducing the ability to resist diseases all right so now we're going to talk about some effects of chronic stress and so this is um basically uh an hpa access and it's a major part of the endocrine system that controls reactions to stress and so what happens is it triggers a set of interactions among the glands hormones and parts of the midbrain that mediate the general adaption syndrome continued stress leads to loss of these normal control mechanisms continued production of cortisol exhausts the stress mechanisms and leads to fatigue and depression consistently high levels of that lead to suppression of the immune system and so stress and depression have a negative effect on the immune system it causes the body to lose its ability to fight disease it encourages the body to release fat and cholesterol into the bloodstream eventually causing heart attacks and strokes it also related conditions include depression headaches insomnia ulcers diuresis acne diabetes mellitus rheumatoid arthritis and asthma coping mechanisms play a role in the um response to stress so healthy persons may manage stress and very little impact on the immune system patients with ineffective coping mechanisms will have detrimental effects on the um immune systems effects are worse on a person with an already compromised immune system okay so this concludes the pathophysiology chapter 9 lecture i hope you've enjoyed it and go ahead and subscribe to the channel if you did we're going to be releasing all the chapters in the the paramedic textbook okay and have a good night