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NUR219 Hematological System
Terms in this set (209)
Blood makes up __% of body weight.
Plasma is __% of blood and formed elements are __% of blood.
3 components of plasma:
water (91% of plasma)
3 formed elements:
platelets, erythrocytes, leukocytes
When you are dehydrated, you have a ___ concentration of hemoglobin and hematocrit.
necessary for regulating the passage of water and solutes through the capillaries
-done at capillary bed on venous side
protect body from disease
Most abundant clotting factor:
promote coagulation and stop bleeding from damaged blood vessels
most abundant cells of the blood
-carry O2 to tissues and cells
fight infection and inflammation
disc shaped cytoplasmic fragments that promote clotting
Primary lymphoid organs:
Secondary lymphoid organs:
peyer patches of small intestine
a large, highly vascular lymphoid organ
-lies to the left of the stomach below the diaphragm
-stores blood, disintegrates old blood cells, filters foreign substances from blood, produces lymphocytes
largest of the secondary lymphoid organs
-not necessary for life or adequate hematologic function
Changes after spleen removal:
decreased iron levels
diminished immune function
blood has more defective cells than normal
structurally part of lymphatic system
functionally part of hematologic and immune systems
-clears foreign particles and m/o
-stimulate resident lymphocytes to develop into antibody producing plasma cells
-macrophages proliferate during infection, swelling them
Functions of the mononuclear phagocyte system:
-mainly found in liver and spleen
-main line of defense against bacteria in blood
-ingest and destroy unwanted materials by phagocytosis
aka myeloid tissue
-in cavity of bone
-has blood vessels, nerves, mononuclear phagocytes, stromal cells, stem cells, blood cells, and fatty tissue
2 kinds of bone marrow:
1. red= active
2. yellow= inactive
T/F: Not all bones contain active (red) marrow.
produce rbc, wbc, and platelets
-fills all bones until age 5 then gradually disappears
-after age 20 it's in ribs, hip bones, femur, shoulder bones and vertebrae. it stays with us throughout life.
fills diaphyses of long bones
-made of connective tissue and large fat cells
-does not normally function hematopoietically, but in pathological processes it can become red/active
takes up oxygen in the lungs and drops it off in other tissues
hemoglobin-containing blood cells
responsible for blood's ruby red color
T/f: Normal development of rbc and synthesis of hemoglobin depends on an optimal biochemical state and adequate supplies.
____ makes red blood cells.
red bone marrow
____ leads to stimulation of kidneys which sends out the hormone _____, which goes into vessels and then bone marrow and tells bone marrow to make more rbc.
hypoxia (low O2)
____ is secreted by the kidney during ____, ___, and ____.
-anemia (low rbc)
-high altitude (less O2 in air)
-pulmonary disease (can't oxygenate)
T/F: Erythropoieten stops secreting when kidneys have had enough.
Receptors that detect hypoxia are in the ____.
Aged rbc are selectively destroyed by the _____. It is primarily done in the ___ but if it is absent, it's done in the liver.
RBC live for ____ days.
120 (4 months)
stoppage of bleeding
2. formation of a platelet plug
3. activation of the clotting cascade
4. formation of a blood clot
5. clot retraction and clot dissolution
Anticoagulants, such as heparin, stop _____ and enhance ___________.
clotting ability and coagulation cascade
fibrin's absorption of thrombin in the clot
an anticoagulant naturally produced by the body
Alterations of rbc function involve either:
1. insufficient or excessive numbers of rbc in circulation
2. normal numbers of cells with abnormal components
-can both cause anemic-type problems
T/f: Anemia is the symptom of another problem.
a reduction in the total number of circulating erythrocytes or a decrease in the quality or quantity of hemoglobin (oxygen-carrying)
____= hemoglobin content
____= varying size
____= assuming various shapes
-small, abnormally shaped erythrocytes
-from lack of iron for hemoglobin production
iron deficiency anemia
T/F: How fast hg and hc drops influences severity of s/s.
S/S of anemia:
possible drop in pulse ox
caused by destruction or depletion of normal erythroblasts or mature erythrocytes
Types of normocytic-normochromic anemia:
anemia from chronic disease/inflammation
caused by decreased stem cell proliferation in the bone marrow (lack of erythropoesis)
caused by accute or chronic bleeding/hemorrhage
-depletes iron stores
caused by premature destruction/lysis of mature erythrocytes in circulation
caused by abnormal hemoglobin synthesis
-abnormal cell shape with suceptability to damage, lysis, and phagocytosis
sickle cell anemia
causes an abnormally increased demand for new erythrocytes
anemia of chronic inflammation/disease
T/f: Anemia that is mild and starts gradually is easier to compensate for and may cause problems for the individual only during physical exertion.
Compensation from anemia involves which systems?
cardiovascular, respiratory, hematologic
Compensation for anemia:
-movement of interstitial fluid into blood (into vascular space)= increases blood volume and bp, decreases viscosity/thins blood
-thin blood causes hyperdynamic state, which increases stroke volume and heart rate
-increased respiratory rate
-RAA activated due to decreased flow to kidneys
-may lead to cardiac dialation and heart valve insufficiency
reduced O2 in blood
-contributes to cardiovascular dysfunction
-increases heart rate and stroke volume due to increased venous return and increased peripheral blood flow
-causes dialation of arterioles and venules
creates additional demands and effects on the pulmonary and hematologic systems
-rate/depth of breathing increases to increase O2
-can lead to dyspnea, rapid/pounding heartbeat, dizziness, and fatigue
T/f: Pale skin, mucous membranes, lips, nail beds, and conjuctiva are also signs of anemia. They could also be yellow because of accumulation of end products of rbc destruction (hemolysis).
Compensatory mechanisms in acute anemia:
-peripheral blood vessel constriction, which diverts flow to essential organs
-RAA system activated due to decreased flow detected by kidneys => causes salt and water retention to increase blood volume
T/F: Long term compensatory mechanisms do not develop for acute anemia.
What is the treatment goal for slowly developing anemia?
treat underlying condition (O2, meds, iron, blood, fluid)
most common type of megaloblastic anemia
-caused by B12 deficiency needed for erythropoesis (caused by lack of intrinsic factor)
-can be fatal
-caused by premature cell death, can be highly injurous
-can lead to abnormal DNA and RNA synthesis in rbc
Who is more affected by pernicious anemia?
common in >30 y/o
-northern european, blacks, hispanics
-females more prone, black females have early onset
What is Vitamin B12 deficiency caused by?
lack of intrinsic factor
-enzyme required for absorption of B12
-this lack can be caused by gastric mucosal atrophy, alcohol, hot tea, smoking
-also associated with autoimmune conditions, especially endocrine
T/F: If you take away part of the stomach during surgery, you lose intrinsic factor.
vitamin required for nuclear maturation and DNA synthesis in rbc
T/f: Individuals with chronic gastritis are at risk for developing gastric cancer.
Pernicious anemia develops ____ over ___ years.
Early symptoms are ____ and include:
-infections, mood swings, GI, cardiac, or kidney ailments
Hallmark sign of pernicious anemia: (appears at 7-8 hemoglobin)
sore tongue that is smooth and beefy red
S/S of pernicious anemia at 7-8 hg:
peristhesias of feet and fingers
loss of appetite
beefy red tongue
sallow skin (lemon yellow)
Evaluation of pernicious anemia:
based on blood tests
-bone marrow aspiration
-gastric biopsy (revelas achlorhydria)
-Schilling test- determines cobalamin absorption; low urine excretion= PA
Untreated pernicious anemia is fatal usually because of ____. Replacement therapy of B12 is needed by injection, at first weekly then monthly for life.
T/F: Pregnant and lactating females need more folate than usual. Folate is gotten through diet.
After absorption, folate circulates and is stored in the ____.
Folate is absorbed from the ______ and does not require anything to facilitate absorption.
upper small intestine
Folate deficiency anemia is caused by:
1. lack of folate for erythropoesis
2. premature cell death
T/F: Folate deficiency occurs more often than B12 deficiency, particular in alcoholics, malnourished, and low vegetable or fad diets. 10% of americans are folate deficient.
Clinical manifestations of folate deficiency anemia:
-cheilosis (scales/fissures of mouth)
-stomatitis (inflammation of mouth)
-painful ulceration of buccal mucosa and tongue
-GI tract changes
-neurologic changes if also thiamine deficiency
Evaluation of folate deficiency anemia:
measure serum folate levels
Treatment of folate deficiency anemia:
long term therapy not necessary
Folate is essential for reducing blood levels of ____ (risk factor for coronary artery disease)
most common anemia in the world
-occurs in developing and developed countries
-high risk: poverty, child bearing age, children
iron deficiency anemia
T/F: Females in the US have a higher incidence than males with IDA with peak incidence occurring in reproductive years and decreasing at menopause.
T/F: During childhood and adolescence, males have a higher incidence of IDA.
T/f: Children under age 2 are often affected by IDA due to increased demand for iron during growth.
____ and ____ are the most common causes of IDA in developed countries.
pregnancy and continuous loss of blood
T/F: A blood loss of 2-4 ml/day is enough to cause IDA.
(tablespoon of blood)
The body is able to recycle iron so a balance is kept between iron used as ____ and iron stored and available for future ____.
Blood loss disrupts this balance by creating a need for more iron, depleting stores more rapidly.
Clinical manifestations of IDA:
-gradual onset of symptoms
-fatigue, weakness, shortness of breath, pale earlobes/palms/conjuctiva
-7-8 hg is when patients come in
Severe symptoms of IDA:
spoon shaped nails (brittle and concave)
tongue papillae atrophy/redness (glossitis)
dry corners of mouth (cheliosis)
Lab findings in IDA:
pale rbc (hypochromic)
small rbc (microcytic)
low serum iron
Evaluation of IDA:
iron stores from lab values or bone marrow biopsy
-find source of blood loss
caused by production of abnormal hemoglobin S within erythrocytes (HbS)
-HbS is formed by genetic mutation in which one amino acid replaces the other, causing sickling of rbc
-inherited, autosomal, recessive
sickle cell anemia
What countries does sickle cell anemia usually occur in?
equatoral countries= central africa, the near east, the mediterranean, and parts of india
In the US, sickle cell is mostly found in ____.
7-13% of african americans
T/f: The sickle cell trait may provide protection against lethal forms of malaria.
A sickled cell can't get through ____ and can't carry ______.
capillaries (so it blocks the vessels)
Sickling depends on the:
-degree of oxygenation
-pH, especially acidic
-dehydration of person
Sickled erythrocytes tend to:
-plug blood vessels (lack of O2 to extremeties/organs)
-increase blood viscosity, causing slow circulation and vascular occlusion, causing pain and organ infarct (no O2 or blood to area)
T/f: High viscosity increases the time of exposure to less oxygenation, promoting further sickling.
T/F: Sickling is usually not permanent.
What can sickling be triggered by?
increased plasma osmolality
decreased plasma volume
low environmental temp
Treatment of sickle cell crisis:
hydration, oxygenation, pain relief
Clinical manifestations of sickle cell anemia:
pain, pallor, fatigue, jaundice, irritability
-vasooccolusive crisis (blood flow obstructed by sickled cells)
-sequestration crisis- blood pooled in liver/spleen
-aplastic crisis- anemia
T/F: Many individuals with sickle cell die in their 30s-40s due to organ damage, MI, stroke, etc.
Treatment of sickle cell:
-avoiding crisis, preventing consequences of anemia
-pain meds, IV hydration
Ex. of a myeloproliferative red cell disorder:
chronic, clonal alteration characterized by overproduction of rbc, wbc, and platelets accompanied by splenomegaly
-mostly occurs in white males of northern european jewish origin 60-80 years
-also observed in females and individuals under 40
neoplastic, nonmalignant condition characterized by deviant, abnormal proliferation of bone marrow stem cells
-overcrowding and occlusion of blood vessels
-underlying cause unknown
Clinical manifestations of polycythemia vera:
clogging and occlusion of blood vessels
tissue injury (ischemia) and death (infarction)
intense, painful itching
plethora (ruddy, red color)
engorgement of retinal/cerebral veins
Evaluation of polycythemia vera:
blood and lab findings with absolute increase in rbc and total blood volume
-high hg and hc
-moderate increase in wbc and platelets
Treatment of polycythemia vera:
-reduce rbc proliferation and blood volume by removing blood
-remove 300-500ml of blood 2-3 times per week until hc levels drop sufficiently.repeat every 3-4 months. hc should be less than 45.
-smokers quit smoking (smoking vasoconstricts, clogging blood vessels)
-preventing of clotting and clogging of vessels
-CHF and COPD may need drug intervention
T/f: Without proper treatment, 50% of individuals with PV die within 18 months of onset of initial symptoms due to thrombosis or hemorrhage.
T/f: In PV, there is a 5x greater chance for death from cerebral thrombosis (stroke).
T/f: PV conversion to acute myeloid leukemia occurs in 10% of individuals.
___ is a normal protective response to physiologic stressors, such as inflammation, infection, and stress.
T/f: Leukopenia is never normal and prevents the ability to fight infection.
an increase in granulocytes (neutrophils, basophils, mast cells, eosinophils)
reduced neutrophil circulation
-severe prolonged infections
-can be caused by leukemia, drugs, anorexia, autoimmune disease, viral infections like HIV, chemo
Neutropenic precautions if count gets too low:
no fresh fruit
increase in eosinophils (>450)
-caused by asthma, hay fever, or drug reactions
an acute infection of b lymphocytes, with Epstein Barr virus (EBV) being most common
-EBV is common in low socioeconomic environments
-early EBV infections are usually asymptomatic and provide immunity
infectious mononucleosis (IM)
T/f: Mono is most commonly seen in ages 15-25 with peak between 15-19.
T/f: Mono is rarely seen in individuals over 40 and if it does, it is often caused by cytomegalovirus (CMV).
Transmission of EBV is usually through _____. It may also be in _______.
saliva or close personal contact
respiratory tract, genital and rectal area, blood
S/S of mono/IM:
-enlarged lymph nodes, tonsils, spleen, and sometimes liver
-30-50 day incubation period
-recovery occurs in few weeks to several months
-pain in RUQ with liver involvement
-headache, malaise, joint pain, and fatigue occur in first 3-5 days
-splenic rupture can occur (more common in males), as well as airway obstruction and autoimmune hemolytic anemia
RUQ pain is from ___
LUQ pain is from ___
Evaluation of mono/im
Treatment of mono/im
-no antibiotic or viral meds
-proper diet, increase protein
-alleviate symptoms with analgesics and antipyretics
-steroids for severe complications
a clonal malignant disorder of the blood and blood forming organs
-causes accumulation of dysfunctional cells and a loss of cell division regulation (cells divide and multiply quickly but are not functional)
-caused by uncontrolled proliferation of leukocytes, causing overcrowding of bone marrow and decreased production of normal hematopoetic cells
Classification of leukemias are based on:
-predominant cell (myeloid-bone or lymphoid)
-point at which cellular maturation is stopped (acute or chronic)
characterized by undifferentiated/immature cells
-onset is abrupt and rapid
-short survival time due to disease progression
______= most common type of leukemia in children and is more than half of all new cases
_____= most common adult acute leukemia
acute lymphoblastic leukemia
acute myelogenous leukemia
Pathophysiology of leukemia
-clonal disorder; a single progenitor cell undergoes transformation
-caused by blocking of differentiation
-both accumulation and slow proliferation
Risk factors for leukemia
acquired disorders (chronic myelogenous leukemia, PV, hodgkins lymphoma, ovarian cancer, large doses of radiation, drugs)
T/F: Incidence of leukemia increases dramatically in those greater than 50 y/o
T/f: Leukemia survival rates for all, especially children, ave increased to 73% due to chemo advances.
Clinical manifestations of acute leukemia:
fatigue from anemia (low hg)
neutropenia- causes risk of infection
thrombocytopenia- bleeding risk
bleeding (skin, gums, mucus membranes, gi tract)
infections due to not functional wbc
anorexia (weight loss, low sensitivity to taste)
liver, spleen, and lymph node enlargement
numerous immature wbc
Treatment of leukemia:
-support by blood transfusions, antibiotic, antifungal, antivirals
bone marrow transplantation
-80-90% survival with complete remission
Tests for leukemia:
bone marrow test
Bone marrow transplantation involves wiping everything from the patient and replacing it with new ______. If the body doesn't react well, the patient may die.
advances slowly and insidiously
-cells well differentiated and can be readily identified
-longer life expectancy
-mostly in adults and over 40 years of age
2 types of chronic leukemia:
chronic myelogenous leukemia= bone
chronic lymphocytic leukemia= lymph
T/f: Individuals with chronic leukemia are usually unaware they have it until symptoms appear.
T/F: Chronic leukemia has a chronic and terminal phase.
-terminal= 30-40 mos. after chronic and survival rate is 3 months
S/s of chronic leukemia:
Treatment of chronic leukemia:
bone marrow transplants
splenectomy to control leukocytosis
radiation for lymphadenopathy
a B cell cancer characterized by the proliferation of malignant plasma cells that aggregate into tumors and distribute throughout the skeletal system
multiple myeloma (mm)
T/f: Multiple myeloma is often accompanied by unknown fractures.
T/f: Multiple myeloma has a higher incidence rate in blacks, has a peak age of 50-60 yrs, is more common in men, and has unknown cause.
Clinical manifestations of multiple myeloma:
Treatment for multiple myeloma:
-survival rate w/ chemo is only 2-3 years
tumors of primary lymphoid tissue (thymus, bone marrow) or secondary lymphoid tissue (lymph nodes, spleen, tonsils, intestinal lymphoid tissue)
have distinctive abnormal chromosomes in multiple cells of lymph nodes
-abnormal cell is called Reed-Sternberg cell
-virus may be involved in pathogenesis
-possible genetic mechanisms
S/s of hodgkin lymphoma:
enlarged, painless mass or swelling most commonly on the neck
Treatment of hodgkin lymphoma:
radiation (shrinks tumor)
-a cure is possible regardless of stage
-poor prognosis if treated and relapse within 2 years
swollen lymph nodes without Reed-Sternberg cell
-higher incidence in immunosuppressed
-can survive for long periods
Treatment of non-hodgkins lymphoma
-may be normal in certain individuals but should not be ignored
Causes of splenomegaly
acute inflammatory or infectious process
tumor or cysts
over activity of the spleen
-results from splenomegaly
-leads to anemia
-treated by removal of spleen
low platelet count below 100,000
-a count below 50,000 increases the potential for hemorrhage even with minor trauma (no tubes, no IM injections)
-concerned about bleeding out
Normal platelet count:
adverse drug reaction to heparin
heparin induced thrombocytopenia (HIT)
platelet count greater than 400,000
-usually asymptomatic until count exceeds 1 million, then they can have thrombosis formation
thrombocythemia (or thrombocytosis)
the ability to promote coagulation and the development of a stable fibrin clot
Impaired hemostasis can be from vitamin __ deficiency.
In ____ disease, clotting factors decrease leading to an increased chance of bleeding.
-have a decrease in platelets and an increase in prothrombin time
____ makes clotting factors, so these patients can bleed out quickly.
DIC stands for _________
disseminated intravascular coagulation
widespread activation of coagulation, resulting in formation of fibrin clots in vessels throughout the body
Clinical manifestations of DIC:
-hemorrhage and vascular lesions
-hematuria, oliguria, renal failure
a clot attached to a vessel wall
-can be arterial or venous
a clot that detaches from the vessel wall and circulates within the blood
-can become lodged somewhere else in the body (heart, lung, brain)
-if lodged it cuts off blood supply and nutrients to the area
Platelets are essential to ____.
____ and ____ will occur with platelet levels less than 20,000.
petichiae and ecchymosis
The most common disease associated with spontaneous thrombocytosis is _____.
Hemorrhage may occur with _____.
Thrombocytosis is seen in:
IDA or hemorrhagic anemia
Thrombocytopenia is seen in:
Normal male and female Hc values:
-slightly decreased in elderly
-critical is <15% or >60%
Hematocrit is usually __ times the hemoglobin concentration
an indirect measurement of rbc number and volume
-percentage of total blood volume that is made up by rbc's
Increased hemoglobin/hematocrit levels:
congenital heart disease
Decreased hemoglobin/hematocrit levels:
bone marrow failure
lymphoma and leukemia
Normal hemoglobin levels for male and female:
-critical value: <5 or >20
vehicle for O2 and CO2 transport
-also important as an acid base buffer
Too little hemoglobin puts strain on the _____ system to maintain good oxygenation. This puts patients at risk for:
angina, MI, CHF, stroke
Higher prothrombin time (PT)/ INR means that blood ________.
takes longer to clot
If there is a blood clot or embolism, we want blood to ____ to prevent more clots.
used to revaluate clotting mechanisms
-measures clotting ability of fibrinogen, prothrombin, etc.
-When these factors are deficient, PT is ____.
____ is a drug that increases PT and INR.
Increased levels of PT:
liver disease, hereditary factor deficiency, vitamin K deficiency, bile duct obstruction, coumadin, DIC, massive blood transfusion
___ is used to access the intrinsic system and common pathway of clot formation. It is also used to monitor heparin therapy.
Partial thromboplastin time (APTT)
Heparin ___ APPT.
APPT ____ with liver disease because it takes longer for blood to clot.
congenital clotting factor deficiencies, cirrhosis of liver, Vitamin K deficiency, DIC, heparin, coumadin
DIC in early stages
If ____ is high, it tells you that there are potential problems with the clotting system and you may have a clot somewhere.
assesses thrombin and plasmin activity
-fibrin degradation fragment made through fibrinolysis
-highly specific measure of the amount of fibrin degredation that occurs
Normal value of d-dimer
Increased levels of D-dimer
crisis in sickle cell
Folic acid is a test used in patients who have ____ anemia. It also assesses nutritional status, especially in alcoholics.
Normal folic acid range:
B vitamin necessary for normal rbc and wbc function
-also for synthesis of DNA and amino acids
Increased folic acid levels:
recent massive blood transfusion
Decreased folic acid levels:
folic acid deficiency anemia
3 causes of anemia:
1. too many erythrocytes
2. too few erythrocytes
3. loss of function of erythrocytes
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