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NR 283 Pathophysiology Exam 3 Concept Review
Hematology RBC-function - Erythrocytes (or RBC’s) are the most abundant cell type in the body Its primary job is tissue oxygenation The cell has 2 unique properties: o A biconcave shape which makes it optimal for gas transport o The capacity to be reversible deformed. The cells can change shape to make it through all the different size vessels in the body Erythrocytes have a lifespan of 120 days Hemoglobin is the oxygen carrying protein of the erythrocyte that gives RBC’s their color Each erythrocyte has over 300 hemoglobin molecules; 1 HGB can carry 4 oxygen molecules Erythropoiesis is the creation of erythrocytes from the bone marrow Erythropoietin-produced, what does it do - Erythropoietin is the hormone that stimulates the production of erythrocytes. o It is produced by the kidneys Epogen (epoetin alpha) is indicated for the treatment of anemia due to chronic kidney disease (CKD), including patients on dialysis and not on dialysis to decrease the need for red blood cell (RBC) transfusion Anemias-types/ S/S of each - Anemia is a decreased total number of erythrocytes or a decrease in the quality or quantity of hemoglobin Causes of anemia are: o Impaired erythrocyte production o Acute or chronic blood loss o An increase in the destruction of erythrocytes o A combination of all 3 Types of anemia
pernicious anemia - It is caused by a vitamin b12 deficiency The main problem is the absence of intrinsic factor which is an enzyme needed to absorb vitamin b12 in the stomach Absence of this factor can be genetic or can be related to problems with the stomach P.A. is most commonly caused by people who have had their stomach or a part of their stomach removed, however a history of alcohol use or smoking can cause it as well PA takes years to develop so initial symptoms can be very non-specific When your hemoglobin starts to be affected (when it decreases) symptoms include weakness, fatigue, and paresthesia’s of feet and hands folate deficiency anemia Folate is another vitamin necessary for DNA synthesis of erythrocytes Folate deficiency anemia is commonly seen in alcoholics and malnourished people With this type, there is no enzyme responsible for making sure we absorb the folate. We are strictly lacking an adequate amount Folate is found in dark, leafy green vegetables, citrus fruits, beans and nuts o Folic acid is a synthesized form of folate Clinical manifestations include: o Cheilosis - fissures and scales in the mouth o Stomatitis- inflammation of the mouth painful ulcers of the tongue Iron deficiency anemia - is the most common type of anemia There are many causes, including insufficient iron in the diet , certain medications, excessive menstrual bleeding in females, or ulcer’s Iron is important because it is used for the production of HGB The development occurs slowly through 3 stages: o Body’s iron stores are depleted. Normal blood cell production occurs o Now insufficient amounts of iron are transported to the marrow where iron deficit RBC’s are produced with low amounts of HGB o The HGB deficient cells enter circulation to replace the normal aging cells that are getting ready to die Clinical manifestations start occurring at stage 3
Tissue injury and death are common as well as a high risk of developing blood clots Another CM is plethora which is a ruddy, red coloring to the face, hands, and mucous membranes A unique CM of PV is a very intense painful itching that only gets worse with exposure to heat or water We mentioned that people with PV also have splenomegaly. Why? What is the spleen’s job? o Remember the spleen’s job is to filter and clean the blood. The more blood you have the harder the spleen has to work, so it grows bigger. o Remember cellular adaptations? Would this be atrophy or hypertrophy? Pathologic or physiologic? Pathologic because it is getting bigger due to an abnormal increase in erythrocytes Secondary polycythemia is another form and results from an increased secretion of erythropoietin from chronic hypoxia (such as people who live at high altitudes where there is less oxygen or patient’s with COPD) We said that if your body senses that you are hypoxic, it will secrete more erythropoietin to create more RBC’s to get more oxygen to the tissues. This is the same thing WBC-quantitative and qualitative-causes - Quantitative alterations refers to an increase or decrease in the amount of leukocytes. Quantitative disorders include: Leukocytosis is an increase in the amount of circulating leukocytes This is a normal response to infection, medications, stress, and medications Neutrophilia is an increase in the number of neutrophils specifically It is seen in the early signs of infection or inflammation Lymphocytosis is an increase in the number of lymphocytes Typically seen in viral infections Leukopenia is a lower than normal amount of circulating leukocytes This can occur in relation to autoimmune diseases or cancer treatments. This is not normal and put someone at a high risk for developing infections Neutropenia is a decrease in the number of neutrophils
This can be associated with long term infections in which the body runs out of neutrophils Lymphycytopenia is a decrease in the number of lymphocytes Is associated with immune deficiencies Can also be related to destruction of the cells from a virus or drug Qualitative alterations affect the ability of the cell itself to function correctly qualitative disorders of leukocytes, starting with leukemia Which is a malignant (cancer) disorder of the blood and the blood forming organs The common feature of leukemia is an uncontrolled growth of malignant leukocytes (leukemic cells) that cause an overcrowding of cells in the bone marrow Because of the overcrowding, pancytopenia (decreased production of all cells) can occur The exact cause of leukemia is unknown but there are risk factors and genetic alterations that are associated with it Leukemia tends to appear in families It also is common in someone who already has a genetic alteration like: o Down’s Syndrome o Gene translocations When two chromosomes break and switch information Other risk factors seen with leukemia include smoking, exposure to radiation, and certain drugs and infections Hodgkin- In Hodgkin Lymphoma a group of B lymphocytes become mutated and grow into abnormally large cells that spread throughout the lymphatic system causing systemic problems Specifically it is the B lymphocyte that is mutated The abnormal B cells, known as Reed Sternberg cells, are the characteristic sign of HL The exact mutation that occurs and why is still unknown However there are some known risk factors for HL that include a history of Mono from the Epstein Barr virus, Family history, male gender, people who are immunocompromised, and age (common 15-35, and 55+) Clinical manifestations of H.L. typically involve NONPAINFUL enlarged lymph nodes that typically start in the neck and are the first sign of H.L.
These malignant plasma cells also like to circulate through the blood and make their way into other bones o So you can have these myelomas throughout your body breaking down bone and tissue Also, normally our plasma cells produce antibodies that help us fight infections These myeloma cells produce antibodies but they are ineffective and cause the individual to have problems fighting infections The most common CM is an increased level of calcium in the blood Other CM’s seen are pain and renal failure as a result of protein in the urine and bone fractures from the destruction of the bone ALTERATIONS IN PLATELETS Thrombocytopenia is a decreased platelet count It can be caused by a decreased production or an increase in consumption of platelets There are 3 types of thrombocytopenia HIT or Heparin Induced Thrombocytopenia- Heparin is a medication known as an anti-coagulant. It thins the blood enough to prevent the production of blood clots HIT is actually a severe drug reaction that is mediated by the immune system In HIT, the body creates antibodies against the heparin These antibodies bind to a protein found on the platelet. The antibody will tell the platelets to aggregate, form a thrombus or clot, and decrease platelet count Often this does not show up until days after the heparin has been given The hallmark sign of HIT is thrombocytopenia that occurs gradually over a matter of days If HIT is not treated right away it can cause people to rapidly develop multiple thrombi which will put them at risk for DVT’s, PE’s, strokes or heart attacks ITP-cause, S/S- ITP or idiopathic thrombocytopenic purpura is another type The cause of ITP is unknown, but it is some kind of abnormality with our immune response For some reason a large amount of antibodies are produced in the blood against thrombocytes
These antibodies will bind to antigens on the surface of the platelet These specific antibody bound platelets are removed from the circulation and destroyed by the spleen CM’s range from minor bleeding issues (purpura and petechiae) to major hemorrhage in a matter of days. Purpura are purple bruises. Petechiae are pinpoint sized red/purple dots on the skin TTP-cause, S/S- TTP or thrombotic thrombocytopenia purpura is a third type of thrombocytopenia This one specifically is a life threatening disorder It is either a genetically inherited disease, or it can be acquired from either an unknown trigger, or such things as lupus or pregnancy It is characterized by thrombotic microangiography which is a disorder of clot formation in capillaries and arteries due to tissue injury o Platelets will spontaneously aggregate o Form micro-thrombi or mini blood clots that rest in arteries and capillaries o And stop blood flow to a specific area of the body A decrease in circulating platelets has occurred because they are all being used to create mini clots throughout the body These mini clots can also prematurely destroy erythrocytes resulting in anemia CM’s are characterized by a set of 5 specific symptoms otherwise known as a pentad o Extreme thrombocytopenia o Intravascular hemolytic anemia o Ischemic signs and symptoms involving mainly the CNS o Kidney failure o Fever ALTERATION IN COAGULATION. DIC-cause, S/S-DIC or disseminated intravascular coagulation is a condition in which the body clots and bleeds at the same time Normally our coagulation and fibrinolytic systems maintain a balance But in DIC, there is a widespread imbalance
Secondary hypertension is caused by another underlying disease process or medication that increased peripheral vascular resistance If the cause is identified and removed before damage occurs, the HTN will resolve itself Complicated hypertension occurs when HTN becomes chronic and more severe over time and can cause tissue damage in the heart, kidneys, brain and eyes Malignant hypertension is a rapidly progressing hypertension If BP is not decreased ASAP, it can lead to organ dysfunction and death Clinical manifestations o Typically only a high blood pressure o CM of organ damage – organ specific o Death o Due to the lack of CM’s, HTN is known as the silent disease or the silent killer In order to diagnose someone with hypertension, they have to have multiple episodes of high blood pressure not R/T other things Atherosclerosis- Atherosclerosis is characterized by hardening + thickening of the vessel wall This is caused by a collection of lipid laden cells on the inner wall of an artery which leads to the formation of a lesion called a plaque Atherosclerosis is not a disease, but a progressive process that can affect vessels anywhere in the body resulting in ischemia Atherosclerosis is the leading cause of CAD and cerebrovascular diseases Risk factors for the development of atherosclerosis include: o Smoking o HTN o DM Orthostatic Hypotension- Orthostatic hypotension is a decrease in the systolic or the diastolic blood pressure upon standing The cause is unknown Normally when you stand, mechanisms like the muscle pump and an increase in HR will compensate for the change in gravity
In orthostatic hypotension, there is something wrong with the body’s ability to compensate for the change in position This causes blood to pool and the BP to drop CM include dizziness, loss of vision, and syncope Thromboembolus- A thrombus is a blood clot that remains attached to a vessel wall. A detached thrombus is a thromboembolus. DVT ( deep venous thrombosis) - A DVT is a blood clot that obstructs the flow of blood When we are looking at risk factors for the formation of a DVT, we use something called Virchow’s Triad , which is a group of 3 factors that promote the formation of DVT: o Venous stasis (slow blood flow in the legs) (immobility, age) o Venous endothelial damage (trauma) o Hypercoagulable states (pregnancy, malignancy, hormone replacement) Clot formation is caused by the accumulation of platelets and clotting factors Inflammation around the thrombus increases its growth The inflammation may cause redness and pain which a patient may C/O However, your patient may not always have symptoms because the clot is in a deep vein. Sometimes the DVT has not made itself known until it has become big enough to occlude blood flow to an extremity and those S/S are what bring your patient into the hospital. PE- Pulmonary embolism is occlusion of a portion of the pulmonary vascular bed by an embolus. PE most commonly results from embolization of a clot from deep venous thrombosis involving the lower leg. A pericardial effusion- is the accumulation of fluid in the pericardial cavity , often seen along with pericarditis Remember I said that there is normally some fluid in the pericardial cavity. In this instance, there is more than normal The fluid can be transudative if the cause is related to heart failure or overhydration In most instances, though, the fluid is transudative, and caused by infections , chemotherapy, or heart surgery If the fluid develops slowly the heart can accommodate for it However, if it occurs quickly it can compress the heart causing a serious condition called tamponade
Modifiable factors, which can be changed, include dyslipidemia, HTN, smoking, DM, Obesity, Sedentary lifestyle, and an atherogenic diet which is high in cholesterol, protein, and fat There are also some nontraditional risk factors They are relatively new and the degree to which they affect CAD is still being explored These include: Presence of serum markers for inflammation Specific levels of certain hormones Certain infections MI- (Myocardial Infarction) There is a multi-step pathologic process that the heart goes through with an infarction The first step is cell injury o 10 seconds after blood flow is decreased, the muscle becomes cyanotic o After oxygen has been depleted, contractility of the heart decreases and electrolyte changes occur The next step is cellular death o Cardiac cells can only live for 20 minutes without oxygen o If oxygen is not returned, cell death and necrosis occurs The 3rd^ step is structural and functional changes of the infected tissue and the tissue surrounding the injured area The final stage is repair of the cells in the area of the injury CM o f infarction include: o Chest pain that is more severe and prolonged than normal (unstable angina) o Pulmonary congestion – crackles o Increased HR and BP Extra heart sound Angina Pectoris (stable, Printzmetal, silent, unstable)- Myocardial ischemia is a temporary loss of blood supply and oxygen to one specific area of the heart The most common cause of ischemia is the formation of atherosclerotic plaques
But can also be caused by anything that decreases oxygen and blood to the tissues, such as hypotension, vasospasm, or presence of a thrombus or embolus Myocardial cells become ischemic in 10 seconds If oxygen is not restored, infarction can occur If blood flow is returned at the right time, the heart will start to contract again and fix any cells that were injured People with reversible ischemia can present with different CM’s: o Stable angina pectoris ( e.g during physical exercise and one starts having chest pain then when you stop the pain goes away) Recurrent, predictable pain The vessel of the heart is starting to narrow and cannot respond to an increase in workload demand So there are people who get pain when exerting themselves o Prinzmetal angina Unpredictable and occurs at rest and with activity Most commonly occurs at night Causes by vasospasm of the vessels, with or without atherosclerosis o Silent Ischemia Totally asymptomatic ischemia More common in women Unstable angina- Chest pain that is more severe and prolonged than normal Acute Pericarditis- is acute inflammation of the pericardium Cause is often idiopathic or due to a viral infection The membrane becomes inflamed and rough, and sometimes a pleural effusion may develop CM include fever followed by chest pain, restlessness, anxiety, and weakness and the presence of a friction rub Constrictive Pericarditis - is associated with TB infections, radiation therapy, and rheumatoid arthritis The pericardium becomes scarred and calcifies, causing the pericardial layers to adhere together causing a loss of the pericardial cavity
It is a febrile illness characterized by inflammation of different parts of the body including joints, skin, and the heart If it is left untreated, it can cause scarring and deformity of cardiac structures (valves) resulting in rheumatic heart disease Infections are mainly found in children Common CM are fever, lymphadenopathy, N/V, epistaxis, abdominal pain and tachycardia Left Heart Failure - Heart failure is when the heart is unable to generate an adequate cardiac output leading to: o Inadequate perfusion of blood and oxygen to the tissues o Increase in the filling pressures of the heart Left heart failure is commonly called Congestive heart failure o Pathophysiologically this is what happens: o It starts with decreased contractility of the heart, usually from an MI o This causes the heart to work harder and the myocardium to become dilated (dilated CMP) o As contractility decreases, preload increases o The heart can’t pump all the blood out effectively, so more remains in the heart, resulting in an increase in preload o Afterload also increases because there is more resistance that the heart has to push against to fully empty o In addition to the heart itself, there are other processes that play a role in the development of heart failure, including: o Immune and inflammatory processes o Dysfunction of the SNS and RAAS (like with HTN) o A vicious cycle of decreased contractility, increased preload, and increased afterload occurs leading to a steady decline of cardiac function, the presence of the CM’s, and eventually death o Manifestations of Left sided heart failure are the result of pulmonary vascular congestion (blood backs up in the lungs) and inadequate perfusion of the systemic circulation
o Dyspnea, orthopnea, cough, frothy sputum, fatigue, edema, pulmonary edema with crackles, hyper or hypotension, heart murmurs o There is also usually evidence of underlying CAD, HTN, or other valvular disease o o Right Heart Failure - (Cor Pulmonale) Right heart failure is an inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal pressure This is most commonly caused by diffuse hypoxic pulmonary disease such as seen with COPD or ARDS It can also result from left sided heart failure Also known as cor pulmonale from the pulmonary chapter QRS Complex (Electroconductivity of the heart)- The QRS complex represents the sum of all ventricular muscle cell depolarization. May vary between individuals. The duration is normally between 0.06 and 0.10 second. During the ST interval , the entire ventricular myocardium is depolarized. The QT interval is sometimes called the “electrical systole” of the ventricles. It lasts about 0.4 second but varies inversely with the heart rate. The T wave represents ventricular repolarization. Renal Pre, Intra, and Postrenal Acute Kidney Injury- acute kidney injury, in which there is a sudden decline in kidney function and a decrease in the GFR and accumulation of waste products in the blood Common causes include: A loss of extracellular fluid either by hemorrhage or dehydration Decreased renal blood flow Injury to the cells of the kidney Acute kidney injury is classified in 3 ways
Chronic Glomerulonephritis - is a kidney disorder caused by slow, cumulative damage and scarring of the tiny blood filters in the kidneys. These filters, known as glomeruli, remove waste products from the blood. In chronic glomerulonephritis, scarring of the glomeruli impedes the filtering process, trapping waste products in the blood while allowing red blood cells or proteins to escape into the urine, eventually producing the characteristic signs of high blood pressure and swelling in the legs and ankles Chronic Kidney Disease- Chronic Kidney Disease is a progressive and irreversible loss of renal function that eventually affects all the systems of the body CKD is commonly associated with HTN, DM, and intrinsic kidney diseases, which are some of the ones we have already talked about: chronic pyelonephritis, chronic glomerulonephritis There are 5 stages of kidney disease that start with normal functioning GFR, to end stage kidney disease With normal functioning , the kidneys filter greater than 90ml of blood per minute By the time the kidneys have reached end stage, they are filtering less than 15ml/minute Whatever the cause of CKD, the end result is the destruction of the functional units of the kidney or the nephrons The kidney will attempt to adapt and compensate for the loss, up until there is over 75% of functioning loss Progression of CKD is associated with the following pathogenic processes: o Glomerular HTN, hyperfiltration, and hypertrophy o This leads to proteinuria o The glomerular HTN is caused by an increase in the production of Angiotensin II which causes vasocontriction o Glomerulosclerosis o Tubule inflammation and fibrosis
Chronic Kidney Disease or Chronic Renal Failure-labs, diagnostics - For kidney disease diagnosis, you may also need certain tests and procedures, such as: Blood tests. Kidney function tests look for the level of waste products, such as creatinine and urea, in your blood. Urine tests. Analyzing a sample of your urine may reveal abnormalities that point to chronic kidney failure and help identify the cause of chronic kidney disease. Imaging tests. Your doctor may use ultrasound to assess your kidneys' structure and size. Other imaging tests may be used in some cases. Removing a sample of kidney tissue for testing. Your doctor may recommend a kidney biopsy to remove a sample of kidney tissue. Kidney biopsy is often done with local anesthesia using a long, thin needle that's inserted through your skin and into your kidney. The biopsy sample is sent to a lab for testing to help determine what's causing your kidney problem. Creatinine and BUN levels- Creatinine is a chemical waste molecule that is generated from muscle metabolism. Creatinine is produced from creatine, a molecule of major importance for energy production in muscles. Approximately 2% of the body's creatine is converted to creatinine every day. Creatinine is transported through the bloodstream to the kidneys. The kidneys filter out most of the creatinine and dispose of it in the urine. The creatinine levels in both urine and blood are determined and compared. Normal creatinine clearance for healthy women is 88-128 mL/min. and 97 to 137 mL/min. in males ( normal levels may vary slightly between labs). Blood urea nitrogen ( BUN ) level is another indicator of kidney function. Acute Cystitis- is inflammation of the bladder and is the most common site of a UTI The most common bacteria that causes cystitis is E.Coli The infection of the bladder causes an inflammatory response The edema from the inflammatory response affects the stretch receptors in the bladder This causes symptoms of fullness when the bladder is only filled with small volumes, thus producing the CM of a UTI CM: Some may be asymptomatic o Frequency o Dysuria (painful urination) o Urgency o Lower abdominal or suprapubic pain
