Week 11: Hematology Flashcards
1
Q
Blood is a fluid composed of?
A
Plasma
RBC
WBC
Platelets
2
Q
physical characteristics of blood
A
- Heavier, thicker, and 3-4 X more viscous than water
- 38o C (100.4oF)
- pH : 7.35 – 7.45
- 4-6 liters in an adult
- Varies with electrolyte concentration and amount of adipose tissue
3
Q
plasma
A
- 92 % Water
- 8% Solutes – organic and inorganic
- Plasma proteins – largest proportion of solutes
- Albumins – 58 % of the proteins – maintain osmotic (oncotic) pressure – hold water in the blood
- Globulins – 38 % - antibodies synthesized by plasma cells
- Clotting factors – fibrinogen – 4 %
4
Q
other components of plasma
A
- Nutrients
- Hormones
- Electrolytes
- Waste products
- Dissolved gases
5
Q
Erythrocytes
A
red blood cells- RBC’s
6
Q
Leukocytes
A
white blood cells – WBC’s
7
Q
Thrombocytes
A
platelets – cell fragments
8
Q
hemapoeisis (hematopoeisis)
A
- All blood cells common from a common stem cell – Hemocytoblast
- These are in the bone marrow (red) and develop into blood cells as needed by the body
- Mitosis is signaled by biochemicals released from the body →
- Stem cell is signaled to differentiate into the needed type of blood cell
- Hematopoiesis / cell breakdown continue through life.
9
Q
erythrocytes (RBC’s)
A
*Most abundant blood cell type
*Transport gases
Shape is important
- Large surface to volume ratio
- Reversible deformability – can change shape
Development is called erythopoiesis
- Erythropoietin is a hormone produced by the kidneys in response to low blood oxygen levels; signals bone marrow to increase RBC production
*RBC’s travel through the body delivering oxygen and removing waste.
*RBC’s are red because they contain a protein chemical called hemoglobin which is bright red in color.
*Hemoglobin contains iron, making it an excellent vehicle for transporting oxygen and carbon dioxide.
*Average life cycle is 120 days.
*The bones are continually producing new cells.
10
Q
Cytoplasm is mostly
A
- hemoglobin (lacks organelles)
- Made up of 4 peptide chains that form the globin portion and four molecules of the pigment heme which contains an atom of iron
- If there is a problem with any part of the molecule it may not be functional.
11
Q
RBC breaksdown
A
- Healthy RBC’s live about 120 days; we break down about 174 million per minute
- RBC’s are removed from circulation by the liver and spleen
- Broken down into heme and globin portions
- Globin is broken down into amino acids
- Iron is removed from heme and stored or recycled
- Heme is broken down into biliverdin and then into bilirubin
12
Q
white blood cells
A
- The battling blood cells.
- The white blood cells are continually on the look out for signs of disease.
- When a germ appears the WBC will:: Produce protective antibodies.Surround it and devour the bacteria.
- WBC life span is from a few days to a few weeks.
- WBC’s will increase when fighting infection.
13
Q
Platelets
A
- Platelets are irregularly-shaped, colorless bodies that are present in blood.
- Their sticky surface lets them form clots to stop bleeding.
14
Q
CBC with differential and platelet count.
A
- Hgb:
- Normal levels are 11 to 16 g / dl
- Panic levels are:
- Less than 5 g / dl
- More than 20 g / dl
15
Q
Normal hematocrit levels
A
- 35 to 44%.
- Panic levels:
- Hmct less than 15 %
- Hmct greater than 60%
16
Q
hemaglobin and hematocrit
A
- Can be used as a simple blood test to screen for anemia.
- The CBC with differential would be used to help diagnose a specific disorder.
- A bone marrow aspiration would be the most conclusive in determining cause of anemia – aplastic / leukemia.
17
Q
bone marrow
A
- Bone marrow is the spongy substance found in the center of the bones.
- It manufactures bone marrow stem cells, which in turn produce blood cells.
- Red blood cells – carry oxygen to tissue
- Platelets – help blood to clot
- White blood cells – fight infection
18
Q
Transfusion
A
- Packed red blood cells – anemia
- Platelets – platelet dysfunction
- Fresh frozen plasma – coagulation factors
19
Q
hemolytic reaction
A
- Refers to an immune response against transfused blood cells.
- Antigens, on the surface of red blood cells, are recognized as “foreign proteins” and can stimulate B lymphocytes to produce antibodies to the red blood cell antigens.
-
Symptoms: Flank pain
Fever
Chills
Bloody urine
Rash
Low blood pressure
Dizziness / fainting
20
Q
nursing management of hemolytic reaction
A
- Stop the blood transfusion.
- Start normal saline infusion. (with new tubing)
- Take vital signs with blood pressure
- Call the MD
- Obtain blood sample and urine specimen.
- Return blood to blood bank.
- Document
21
Q
febrile reaction
A
- Often occurs after multiple blood transfusions.
- Symptoms:fever, chills, and diaphoresis.
- Interventions:
- Slow transfusion and administer antipyretic.
- Administer antipyretic prior to administration.
22
Q
allergic reaction
A
- Symptoms: rash, urticaria, respiratory distress, or anaphylaxis.
- Interventions:administer antihistamine before transfusion. Physician may order washed rbc’s
- What should you do? Stop the infusion. Call provider and ask what they want you to do.
23
Q
The following have a genetic link: implications for genetic screening and fetal diagnosis
A
- Sickle cell anemia
- Thalassemia
- Hemophilia
24
Q
Three types Hemophilia
A
- males only
- Type A most common – factor VIII deficiency
- Type B - lack of factor IX (Christmas Disease) (2nd most common)
- Type C – lack of factor XI
- Von Willebrand Disease – 1% of population – men or women – prolonged bleeding time. Significant for women who go on birthcontrol. If they have this and go on bc they end up stroking.
25
Q
hemopheilia type A
A
- is the deficiency of clotting factor VIII.
- A serious blood disorder
- Affects 1 in 10,000 males in the US
- Autoimmune disorder with lowered level of clotting factor
- All races and socio economic groups affected equally
- Hemophilia is a sex-linked hereditary bleeding disorder
- Transmitted on the X chromosome
- Female is the carrier
- Women do not suffer from the disease itself
- First recorded case in Talmud Jewish text by an Arab physician – documentation of two brothers with bleeding after circumcision.
- Queen Victoria was a carrier and spread the disease through the male English royalty.
26
Q
goals of care for hemophilia
A
- Provide factor VIII (IX) to aid blood in clotting.
- To decrease transmission of infectious agents in blood products; hepatitis & AIDS.
- Future: gene therapy to increase production of clotting factor.
27
Q
symptoms of hemophilia
A
- First identified in infancy/childhood
- Circumcision may produce prolonged bleeding.
- As child matures and becomes more active the incidence of bleeding due to trauma increases
- May be mild, moderate or severe
- Bleeding into joint spaces, hemarthrosis
- Most dangerous bleed would be intracranial.
*
28
Q
diagnosis,treatment, and nursing diagnosis/interventions of hemophilia
A
Diagnosis
- Presenting symptoms
- Prolonged activated aPTT and decreased levels of factor VIII or IX.
- Genetic testing to identify carriers
Treatment
- Fresh frozen plasma and cryoprecipitate which are from single blood donors and require special freezing.
- Second generation of factor VIII are made with animal or human proteins.
- Pt;s with severe hemophilia given helmets to prevent falling, hitting their heads, and getting a bleed
Nursing Diagnosis
- Risk for injury
- Pain with bleed especially into a joint
- Impaired physical mobility
- Knowledge deficit regarding disease and management of disease
Nursing Intervention
- No rectal temps.
- Replace the factor as ordered by physician.
- Manage pain utilizing analgesics as ordered.
- Maintaining joint integrity during acute phase: immobilization, elevation, ice.
- Physical therapy to prevent flexion contraction and to strengthen muscles and joints.
- Provide opportunities for normal growth and development.
29
Q
teaching for hemophilia
A
- Avoid aspirin which prolongs bleeding time in people with normal levels of factor VIII.
- A fresh bleeding episode can start if the clot becomes dislodged.
- Natural reactions in the body cause the clot that is no longer needed to “break down. This process occurs 5 days after the initial clot is formed.
30
Q
family education for hemophilia
A
- Medic-Alert bracelet
- Injury prevention appropriate for age
- Signs and symptoms of internal bleeding or hemarthrosis
- Dental checkups
- Medication administration
31
Q
long term complications of hemophilia
A
- 20% develop neutralizing antibodies that make replacement products less effective.
- Gene therapy providing continuous production of the deficient clotting factor could be the next major advance in hemophilia treatment.
32
Q
DIC, what is it and assessment findings
A
- DIC is an acquired coagulopathy that is characterized by both thrombosis and hemorrhage.
- DIC is not a primary disorder but occurs as a result of a variety of alterations in health.
Assessment findings
- The most obvious clinical feature of DIC is bleeding.
- Renal involvement = hematuria, oliguria, and anuria.
- Pulmonary involvement = hemoptysis, tachypnea, dyspnea and chest pain.
- Cutaneous involvement = petechiae, ecchymosis, jaundice, acrocyanosis and gangrene.
- If they survive it will be altering physically for them
33
Q
management of DIC
A
- Treatment of the precipitating disorder.
- Supportive care with administration of platelet concentration and fresh frozen plasma and coagulation factors.
- Administration of heparin (controversial in children).
- Heparin potentates anti-thrombin III which inhibits thrombin and further development of thrombosis.
34
Q
nursing diagnosis and intervention of DIC
A
Nursing Diagnosis
- Altered tissue perfusion
- Risk for injury
- Anxiety
Nursing Interventions
- Rigorous ongoing assessment of all body systems
- Monitor bleeding
- No rectal temps
- Avoid trauma to delicate tissue areas
- All injections sites and IV sites need to be treated like an arterial stick.
35
Q
Idiopathic thrombocytopenia purpura
A
- Idiopathic = cause is unknown
- Thrombocytopenic = blood does not have enough platelets
- Purpura = excessive bleeding / bruising
- Antibodies destroy platelets
- Antibodies see platelets as bacteria and work to eliminate them
- ITP is preceded by a viral illness: URI, Varicella / measles vaccine, Mononucleosis, Flu
36
Q
Symptoms, diagnostic tests of ITP
A
Symptoms
- Random purpura
- Epistaxis, hematuria, hematemesis, and menorrhagia
- Petechiae and hemorrhagic bullae in mouth
Diagnostic tests
- Low platelet count
- Peripheral blood smear
- Antiplatelet antibodies
37
Q
normal platelet count
A
Normal platelet count: 150,000 to 400,000
38
Q
managment of ITP
A
- IV gamma globulin to block antibody production, reduce autoimmune problem
- Corticosteroids to reduce inflammatory process
- IV anti-D to stimulate platelet production
39
Q
Sickle Cell Anemia
A
- Autosomal recessive disorder
- Defect in hemoglobin molecule
- Cells become sickle shaped and rigid
- Lose ability to adapt shape to surroundings.
- Sickling may be triggered by fever and emotional or physical stress
- Patho: When exposed to diminished levels of oxygen, the hemoglobin in the RBC develops a sickle or crescent shape; the cells are rigid and obstruct capillary blood flow, leading to congestion and tissue hypoxia; clinically, this hypoxia causes additional sickling and extensive infarctions.
40
Q
body systems affected by sickle cell
A
- Brain: CVA – paralysis - death
- Eyes: retinopathy – blindness
- Lungs: pneumonia
- Abdomen: pain, hepatomegaly, splenomegaly (medical emergency due to possible rupture
- Skeletal: joint pain, bone pain – osteomyelitis
- Skin: chronic ulcers – poor wound healing
41
Q
vaso-occlusive crisis
A
- Stasis of blood with clumping of cell in the microcirculation, ischemia, and infarction
- Most common type of crisis; painful
- Signs include fever, pain, tissue engorgement
42
Q
splenic sequestration
A
- Life-threatening / death within hours
- Pooling of blood in the spleen
- Signs include profound anemia, hypovolemia, and shock
- Abdominal distention, pallor, dyspnea, tachycardia, and hypotension
43
Q
aplastic crisis
A
- Diminished production and increased destruction of red blood cells
- Triggered by viral infection or depletion of folic acid
- Signs include profound anemia, pallor
44
Q
nursing diagnosis/managment for sickle cell
A
Nursing Diagnosis
- Altered tissue perfusion
- Pain
- Risk for infection
- Knowledge deficit regarding disease process
Nursing Managment
*Increase tissue perfusion
- Oxygen
- Blood transfusion if ordered
- Bed rest
*Pain management
*Hydration
- IV fluids as ordered
- Oral intake of fluids
*Adequate nutrition
*Emotional Support
*Discharge instructions
- Information about disease management
- Daily folic acid
- Control of triggers
- Prophylactic antibiotics
- Immunizations / Pneumococcal
45
Q
patient education for sickle cell
A
- Necessity of following plan of care
- Signs and symptoms of impending crisis (SOB, fatigue, fever)
- Signs and symptoms of infection
- Preventing hypoxia from physical and emotional stress
- Proving adequate rest
46
Q
Beta-Thalessemia
A
- Hereditary / autosomal defect
- Genetic defect on chromosome 11
- Mediterranean descent
- Defect in the beta globin gene
- Beta globin chains are required for synthesis of hemoglobin A
- Beta thalassemia is classified into two types depending on the severity of symptoms:
- thalassemia major (also known as Cooley’s anemia) most life threateningThe child born with thalassemia major has two genes for beta thalassemia and no normal beta-chain gene. The child is homozygous for beta thalassemia. This causes a striking deficiency in beta chain production and in the production of Hb A. Thalassemia major is, therefore, a serious disease.
- thalassemia intermedia.
47
Q
RBC characteristics in Beta-Thalessemia
A
- Microcytosis = small in size
- Hypochromia = decrease hemoglobin
- Poikilocytosis = abnormal shape
48
Q
treatment of beta-thalessemia
A
- Supportive
- Blood transfusions as needed
- Worry about iron build-up
- Bone marrow transplant
- Gene therapy- forefront
- Poor prognosis / death within 1st year due to septicemia or heart failure.
49
Q
Anemia
A
- is the inability of the blood to carry sufficient oxygen to the body.
- low #’s of RBCs
- lack of hemoglobin
50
Q
clinical manifestation of anemia
A
- Pallor
- Fatigue
- Pallor
- Weakness; exercise intolerance
- Dyspnea
- Syncope (fainting) and dizziness
- Angina
- Tachycardia (increased heart rate)
- Organ dysfunctions
- Heart failure
51
Q
classification of anemias
A
- Identified by their causes or by the changes that affect the size, shape or substance of the erythrocyte
- Terms that end with –cytic refer to cell size, and those that end in –chromic refer to hemoglobin content.
- Additional terms:
- Anisocytosis – various sizes
- Poikilocytosis – various shapes
52
Q
macrocytic/megaloblastic anemia
A
- Characterized by abnormally large stem cells (megaloblasts) in the marrow that mature into erythrocytes that are unusually large in size, thickness and volume. The hemoglobin content is normal, so these are normochromic anemias.
- These anemias are the result of:
- Ineffective DNA synthesis
- Commonly due to folate and B12 (cobalamin) deficiencies – malabsorption or malnutrition
- These cells die prematurely, decreasing the numbers of RBC’s in circulation
- DNA synthesis is blocked or delayed, but RNA replication and protein synthesis are normal.
53
Q
pernicious anemia
A
- Common megaloblastic anemia
- Caused by a Vitamin B12 deficiency
- Pernicious means highly injurious or destructive – this condition was once fatal
- Can be congenital – baby born with a deficiency in a protein , intrinsic factor, necessary to absorb B12 from the stomach
- Adult onset – one example is an autoimmune dysfunction -
- type A chronic atrophic gastritis – where there is destruction of the gastric mucosa
- Most commonly affects people over 30
- Females are more prone to PA
- AA females have an earlier onset.
- Develops slowly – over 20 - 30 years
- Usually severe by the time individual seeks treatment
- Early symptoms ignored because they are nonspecific and vague- infections, mood swings, and gastrointestinal, cardiac or kidney ailments.
- Usually a degree of neuropathy occurs
- Untreated, it is fatal, usually due to heart failure
54
Q
Pernicious Anemia is also associated with
A
- Heavy alcohol consumption
- Hot tea
- Cigarette smoking
- Other autoimmune conditions
- Complete or partial removal of the stomach can cause intrinsic factor deficiency
55
Q
folate deficiency anemia
A
- Folic acid also needed for DNA synthesis
- Demands are increased in pregnant and lactating females
- Absorbed from small intestine and does not require any other elements for absorption.
- Folate deficiency is more common than B12 deficiency
- Folate deficiency is more common in alcoholics and those who are malnourished because of fad diets or diets low in vegetables.
- Estimated that 10 % of North Americans are folate deficient.
56
Q
Specific manifestations of Folate deficiency
A
cheilosis (scales and fissures of the mouth), inflammation of the mouth, and ulceration of the buccal mucosa and tongue.
57
Q
microcytic-hypochromic anemias
A
Characterized by abnormally small RBC’s that contain reduced amounts of hemoglobin.
Possible causes:
- Disorders of iron metabolism
- Disorders of porphyrin and heme synthesis
- Disorders of globin synthesis
58
Q
iron deficiency anemia
A
Most common nutritional deficiency
Depletion of iron stores
Most common type of anemia throughout the world.
High risk:
- Individuals living in poverty
- Females of childbearing age
- Children
Common causes
- Insufficient iron intake
- Chronic blood loss – even 2- 4 ml/ day
- In men –gastrointestinal bleeding
- In women – profuse menstruation, pregnancy
Other causes
- Use of medications that cause GI bleeding
- Surgical procedures that decrease stomach acidity, intestinal transit time, and absorption
- Eating disorder
59
Q
clinical manifestations
A
- Early symptoms are nonspecific (pica)
- Later - changes in epithelial tissue:
- Fingernails become brittle and concave (koilonychia)
- Tongue papillae atrophy and cause soreness, redness and burning
- Corners of mouth become dry and sore
- Difficulty in swallowing due to web of mucus and inflammatory cells at opening of esophagus
60
Q
abnormal lab values of iron deficiency anemia
A
- Hemoglobin levels less than 8 g/dL
- Decreased levels of Serum Iron or Total Iron Binding or Serum Ferritin
- Microcytic and hypochromic red blood cells
61
Q
iron deficiency anemia occurs in?
A
- Children during rapid physical growth
- Low iron intake
- Inadequate iron absorption
- Loss of blood
62
Q
symptoms iron deficiency anemia
A
- Pallor
- Fatigue
- Shortness or breath
- Irritability
- Intolerance of physical work / exercise
63
Q
managmenet of iron deficience anemia
A
Iron supplementation
- Given in a.m. on an empty stomach
- In Pediatrics: To avoid staining of teeth, give using a syringe, dropper or straw
- Dark-colored stools
- Constipation
- Nutritional counseling
- Infants younger than 12 months should be on formula until around 12 months of age
- Infants 12 months or older: Decrease intake of milk, Introduce solid foods
- Children- Adults: iron fortified cereals, foods, meat, green leafy vegetables
*
64
Q
sideroblastic anemia
A
- Due to inefficient iron uptake, resulting in abnormal hemoglobin synthesis
- Characterized by the presence of ringed sideroblasts in the bone marrow – red cells containing iron granules that have not been synthesized into hemoglobin, but instead are arranged in a circle around the nucleus.
- Can be acquired or hereditary
- Acquired SA is the most common
- May be idiopathic or associated with other disorders
- Reversible - secondary to alcoholism, drug reactions, copper deficiency and hypothermia
- Hereditary SA –rare, almost always in males – probably X-linked recessive gene.
*
65
Q
clinical manifestation of sideroblastic anemia
A
Along with cardiovascular and respiratory manifestations of anemia, may also show signs of iron overload (hemosiderosis)
- Enlargement of spleen and liver
- Bronze tint to skin
- Heart rhythm disturbances
- Impaired growth and development in young children
66
Q
treatment of sideroblastic anemia
A
- Drug therapy – pyridoxine (B6)
- Iron overload requires repeated blood removal – phlebotomies
- Iron chelating agents in anemic individuals who require transfusions
67
Q
normocytic anemia
A
- RBC’s are normal in size and hemoglobin content, but are too few in number.
- Less common than the macrocytic and microcytic anemias
- Several types that do not have anything else in common:
- Aplastic
- Posthemorrhagic
- Hemolytic – covered with genetic link blood disorders
- Sickle cell - covered with genetic link blood disorders
68
Q
aplastic anemia and causes
A
- Acquired or inherited
- Normal production of blood cells in the bone marrow is absent or decreased.
- A marked decrease in RBC’s, WBC’s and platelets.
Causes
- Exposure to drugs
- Exposure to chemicals
- Exposure to toxins
- Infection
- Idiopathic in nature
69
Q
blood characterstics of aplastic anemia
A
- Neutophil less than 500
- Platelet less than 20,000
- Hemoglobin less than 7
- Reticulocytes 1%
- Bone marrow reveals hypo-cellular and fatty marrow.
70
Q
nursing diagnosis
A
- decreased oxygen carrying ability of rbc’s
- risk of bleeding
- risk of infection
71
Q
managmenet of aplastic anemia
A
- Immunosuppressive therapy
- Antithymocyte globulin
Administered IV over 4 days
Response seen within 3 months
- Bone Marrow Transplant
72
Q
posthemorrhagic anemia
A
- Caused by sudden loss of blood.
- Can be fatal if loss exceeds 40- 50 % of plasma volume.
- Treatment is to restore blood volume by intravenous administration of saline, dextran, albumin, plasma or whole blood.
73
Q
myeloproliferative disorders
A
- The opposite of anemias –here we have too many RBC’s.
- Polycythemia – excessive production of RBC’s
- Primary polycythemia – cause is unknown, but is in effect, a benign tumor of the marrow, leading to increased numbers of stem cells and therefore RBC’s, and splenomegally.
- Polycythemia vera – rare, mostly Northern European Jewish males between 60 – 80 yrs.
74
Q
secondary polycythemia
A
- Due to the overproduction of erythropoietin caused by hypoxia. This is more common.
- Seen in:
- Persons living at high altitudes
- Smokers
- COPD patients
- Congestive heart failure patients
75
Q
Polcythemia leads to
A
- Increased blood volume and viscosity
- Congestion of liver and spleen
- Clotting
- Thrombus formation
- (last two may be due increased numbers of platelets along with the increase in RBC’s due to bone marrow dysfunction.)
76
Q
A
erithromyelalgia (polycythemia finding)
77
Q
clinical manifestations of polycythemia
A
- Headache
- Dizziness
- Weakness
- Increased blood pressure
- Itching / sweating
78
Q
treatment of polycythemia
A
- Reduce blood volume by phlebotomy – 300-500 ml.
- Treat underlying condition - Stop smoking
- Chemotherapy
- Radioactive phosphorus injections
- Prevent thrombosis
79
Q
hyperbilirubinemia S/S
A
- Very yellow or orange skin tones (beginning at the head and spreading to the toes)
- Increased sleepiness, so much that it is hard to wake the baby
- High-pitched cry
- Poor sucking or nursing
- Weakness, limpness, or floppiness
80
Q
nursing interventions of hyperbilirubinemia
A
- Monitor bilirubin levels
- Assess activity level – muscle tone – infant reflexes
- Encourage oral intake: May need to supplement with formula if inadequate breastfeeding
- Weight daily to assess hydration status
- Monitor stools – amount and number
- Cover eyes while under bili-lights
- Facilitate parent - infant bonding
81
Q
how do we assess jaundice on baby
A
- sclera
- hands and feet
- yellow that doesn’t go away when we blanch it
82
Q
kernicterus findings
A
- Loss of moro or startle reflex can indicate possible brain damage due to Kernicterus
- bili levels have gone so high they’ve actually crossed blood/brain barrier
