NR 283 Exam 3 Concept Review
NR 283 Exam 3 Concept Review
Hematology
RBC-function- Erythrocytes (or RBC’s) are the most abundant cell type in the
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• 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
• Early symptoms are non-specific including fatigue, weakness, and SOB
• As it become more severe, clinical manifestations can include:
o Koilonychias - the fingernails become brittle and concave or spoon shaped
o the tongue becomes sore and reddened
o the corners of the mouth become dry and sore
Sideroblastic anemia -is another type of anemia
• It is characterized by a problem with the synthesis or creation of HGB
• In SA, there is plenty of iron, but it is not used correctly to make the HGB
• The erythrocytes end up with a little bit of HGB and a circle of iron in the RBC itself
• SA’s can be classified as:
o Acquired: the most common and are idiopathic (no known cause)
o Hereditary: this is rare and is almost always found in men
o Reversible: this is associated with alcoholism because the alcohol impairs heme synthesis
• CM’s include those commonly seen with anemia
• These people will also have signs of a syndrome called hemosiderosis or iron overload
Enlarged liver/spleen, deposits of iron in heart affecting its function
Polycythemia Vera- polycythemia which is the term for an excess production of RBC’s
• There are many forms of Polycythemia
• The main one I will focus on is primary absolute polycythemia, also known as Polycythemia Vera.
• The main cause is unknown but thought to be due to a genetic alteration of the erythrocyte receptor
o So the receptor is not sensing that there are enough circulating erythrocytes and just keeps producing them
• The clinical manifestations of PV are due to an increase in the viscosity or thickness of the blood
o The number of blood cells increase in the vessel but the amount of plasma or fluid does not so you have an overcrowded vessel which makes the blood very thick
• This can cause clogging and occlusion of blood vessels (think congested highways)
• 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.
• Other CM’s include fever without signs of infection, pruritus, and fatigue and Non-Hodgkin lymphoma, differences
Non-Hodgkin’s lymphoma is actually a general term used to describe lymphomas of other types of lymphocytes (B, T, and NK lymphocytes)
• They are different from H.L. in that they :
• don’t have the reed-Sternberg cells
• their cellular changes are different
• But they are both cancers of the lymphocytes of the lymph system
• Like other cancers, NHL come from gene mutations, specifically gene translocations
• Risk factors for NHL include family history, exposure to chemicals, certain viruses, and immunosuppression
• NHL is more common than HL, and typically does not show up until later in life
• CM’s usually start with painless swelling of lymph nodes other than the neck. The swelling can occur over months to years. Other CM’s can include abdominal or bone pain
• One specific type of NHL is Multiple myeloma
Infectious Mononucleosis- Infectious mononucleosis is an infection of a specific type of lymphocyte called a B lymphocytes by the Epstein Barr virus
• This is known as the kissing disease and is common in colleges because it is transmitted through saliva from close personal contact
• The infection starts when the EBV attacks some of the B lymphocytes and damage and destroy them
• Unaffected B cells will produce antibodies against the EBV and then attack it.
• This is why the disease is self-limiting because it can stop it itself
• Initial CM’s include flu-like symptoms such as fever, fatigue, and joint pain
As mono progresses, lymph nodes can get bigger
Multiple Myeloma- is the growth of malignant plasma cells (type of WBC) that invade bone marrow and form into tumors inside of bones
• The cells have been mutated by chromosome translocations or deletions
• Once a large enough group of cells aggregate together, they enter the bone and activate osteoclasts that break down the bone and release the calcium into the circulation.
• 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
• The most common cause of DIC is a bacterial infection or sepsis
o However it can also be caused by trauma, cancer, or severe hypoxia
• What happens is there is an extensive amount of something called tissue factor
• Tissue factor is released from cells after some kind of tissue injury (hence bacterial infections being the major cause)
• Tissue factor normally activates the extrinsic pathway of the coagulation cascade
• Because there is an extensive amount of it, the coagulation cascade is continuously activated
• This causes small blood clots to be formed all over the body
• And because the coagulation cascade is constantly being activated and clots being made, eventually the body will use up all of its platelets, clotting factors, and coagulation proteins
• Now normal coagulation is affected, which causes the bleeding to occur
• And because the coagulation factors are gone, bleeding cannot stop
Cardiovascular
Hypertension- Hypertension is increased arterial blood pressure
• It is the most commonly diagnosed disease in the US
• Most common in adults but starting to occur in kids
• Primary hypertension is the most common type of hypertension
• The specific cause is unknown
• However there seems to be a combination of genetic and environmental factors that may lead to the development of HTN
• Risk factors include family history, increased age, gender, black race, high sodium intake, smoking, obesity, etc.
• HTN results from a sustained increase in :
o Peripheral resistance (aka arterial vasoconstriction), +/or
o an increase in the volume of circulating blood
Pathologically, there are many mechanisms and factors that combined result in hypertension
• 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
• Tamponade is so dangerous because it affects the ability of the heart to fully fill with blood
• Because there is less blood and oxygen being pushed out, this will lead to a decrease in cardiac output and circulatory collapse due to a lack of blood in the system
• The hallmark sign of tamponade is pulsus paradoxus
Significant drop (greater than normal) in SBP during inspiration
Raynaud’s Phenomenon
Varicose Veins- A varicose vein is a vein in which blood has pooled, producing distended, tortuous and palpable veins
• Risk factors include age, female gender, family history, obesity, pregnancy, and previous leg injury
• They can be caused by trauma to a vein that damages one of the valves
o When the valve is damaged that part of the vein is susceptible to larger volumes of blood pooling because of gravity
• Varicose veins can also be caused from gradual venous distension in people who are on their feet a lot
o Blood pools in the legs frequently due to gravity
• Whatever the cause, the vein gets swollen and filled with blood, which then causes the surrounding tissues to become edematous
CAD- Coronary artery disease, myocardial ischemia, acute coronary syndrome, and myocardial infarction are a continuum of disease that impair the pumping ability of the heart by depriving it of oxygen and nutrients
• Atherosclerosis is the most common cause of all 4
• Diagnosis of atherosclerosis and the continuum of disease is typically done through EKG, stress tests, echocardiograms, CT scans, or cardiac angiograms
• The earliest lesions are those of CAD
• CAD decreases blood and oxygen supply until ischemia occurs
• CAD causes 1 in 6 deaths in the United states
• The risk factors for CAD are classified as major and modifiable
• Major factors, which cannot be changed, include increased age, male gender, female gender after menopause, and family history
• 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 of 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 [Show Less]