Hematology/Neoplasms Flashcards
a test to measure Hgb S
hemoglobin electrophoresis
low hemoglobin and hematocrit, small red blood cells, and an increased total iron binding capacity are all signs of…
iron deficiency anemia
lab test used to to evaluate red blood cell size
mean corpuscular volume
best laboratory test for detecting a clotting factor defect
aPTT
beta thalassemia minor, the genetic defect is in the ________
Hemoglobin
Cancers arise in cells that have alterations in the ______
genes
these are high at birth & cont to rise in some healthy infants during the 1st yr of life; steady decline occurs throughout childhood and adolescence until adult values reached
lymphocytes (neutrophils, eosinophils, monocytes)
For full-term neonates: these are comparable to counts in adults and remain so throughout infancy and childhood
platelets
normal erythrocyte life span in full-term infants
60-80 days
normal erythrocyte life span in pre-term infants
20-30 days
erythrocytes have many ______ in full-term infants
reticulytes
normal erythrocyte life span in children/adolescents/adults
120 days
aging causes erythrocytes to ________ while maintaining normal lifespan
replenish more slowly
Causes of \_\_\_\_\_\_\_ in Aging Fe++ depletion Decreased total serum Fe++ Decreased Fe++ binding capacity Decreased intestinal Fe++ absorption
erythrocyte replacement slowing
Signs of \_\_\_\_\_\_\_ in the hematological system: Platelet adhesiveness increases Lymphocyte function decreases T-cell function declines Humoral system less responsive
Aging
large cells with normal Hgb
macrocytic normochromic anemias
Risk Factors for \_\_\_\_\_\_\_\_: Dietary deficiency alcoholism cirrhosis malabsorption increased requirement state (pregnancy)
folate anemia
low maternal folate leads to ______
neural tube defects
Lab Findings in ________:
- Low RBC
- Low Reticulocytes
- Low WBC
- Low Plt
- Low serum Folate
- High MCV
- High Homocysteine
- Normal MCHC / MCH
- Normal methylmalonic acid
folate anemia
Folate deficiency leads to abnormal _______ in RBC (as in B12 deficiency)
DNA synthesis
Both ________ have defective DNA synthesis in the bone marrow
folate and B12 anemia
Clinical Manifestation of \_\_\_\_\_\_\_: Mild: fatigue weakness lethargy pale skin irritability SOB (nonspecific and vague) Severe: cheilosis (scales and fissures of the lips and corners of the mouth) stomatitis (inflammation of mouth) painful ulcerations of buccal mucosa & tongue (burning mouth syndrome) dysphagia flatulence watery diarrhea ***Generally don’t see neurologic or psychiatric manifestations**
Folate Anemia
condition with high MCV: the RBC’s are large w/ normal Hgb, MCHC, MCH
macrocytic anemia
a measure of the concentration of haemoglobin in a given volume of packed red blood cel
mean corpuscular hemoglobin concentration (MCHC)
average mass of hemoglobin per red blood cell in a sample of blood
mean corpuscular hemoglobin (MCH)
Autoimmune disorder that causes destruction of the parietal cells in the stomach with complete loss of intrinsic factor
Pernicious (B12 Deficiency) Anemia
enzyme that is necessary for the absorption of B12
intrinsic factor
Risk Factors for \_\_\_\_\_\_: Alcoholism cirrhosis bariatric surgery H. pylori medications (H2 blockers, proton pump inhibitors)
Pernicious (B12 Deficiency) Anemia
ineffective DNA synthesis in RBC production in bone marrow that produces megaloblasts that do not mature properly and die off early (happens slowly)
B12 deficiency patho
_____ mostly affects older women (median age = 60)
Pernicious (B12 Deficiency) Anemia
Lab Findings of \_\_\_\_\_\_\_ Low RBC Low Reticulocytes Low WBC Low Plt - High MCV - High homocysteine - High methylmalonic acid -Normal MCHC / MCH -Norm-low serum cobalamine (B12)
Pernicious (B12 Deficiency) Anemia
methylmalonic acid is high in pernicious anemia because…
B12 is needed to break it down
Clinical Manifestations of ________:
vague, nonspecific sx (similar to folate deficiency)
Severe cases: marked anemia & neurological deficits
Marked anemia:
-Weakness, fatigue
-Paresthesias of feet & fingers
-Difficulty walking
-Loss of appetite
-Abdominal pain
Neurological deficits:
-Peripheral nerve degeneration is r/t demyelinating lesions of spinal cord & cerebral cortex
-myelin degeneration & loss of nerve fibers in the dorsal and lateral columns of the spinal column and cerebral cortex
***Megaloblastic Madness
Delusions, hallucinations, outbursts, paranoid schizo ideation
Pernicious (B12 Deficiency) Anemia
small cell size with decreased Hgb
MCV, MCHC low
Microcytic Hypochromic Anemia
Causes of \_\_\_\_\_\_\_: Nutritional deficiency blood loss (slow-GI bleed, fast-hemorrhage) Less common: decreased GI absorption pregnancy renal failure
Iron Deficiency Anemia
______ results in pale, small RBCs with lower than normal Hgb concentration
Iron Deficiency Anemia
Lab Findings of \_\_\_\_\_\_: Low Hgb concentration Low reticulocytes Low RBCs Low MCV, MCH /MCHC Low serum Ferritin Low serum Fe++ Increased total Fe++ binding capacity
Iron Deficiency Anemia
Clinical Manifestations of \_\_\_\_\_\_\_: (s/sx depends on severity) Mild-moderate: no sx (explore hx of any bleeding or s/s of bleeding) Severe: fatigue headache palpitations decreased exercise tolerance weakness More advanced: sore tongue brittle or spoon-shaped nails (koilonychia) PICA
Iron Deficiency Anemia
Normal cell size and Hgb
Normochromic/Normocytic Anemias
anemia caused by accelerated destruction of RBCs in which Erythrocyte production is unable to keep up with destruction
Hemolytic Anemia
type of hemolytic anemia that occurs due to deficiency in CD55 and CD59, a complement mediated intravascular lysis of RBCs & release of Hgb
Paroxysmal nocturnal hemoglobinuria
type of hemolytic anemia in which autoantibodies against antigens normally on the surface of the erythrocyte are present:
• Warm reactive antibody type
• Cold agglutinin type
• Cold hemolysin type (paroxysmal cold hemoglobinuria)
**named according to the optimal temperature at which the antibody binds to the erythrocyte
Autoimmune hemolytic anemias
type of hemolytic anemia that is due to an allergic rxn against foreign antigens: the drug (penicillin, cephalosporins, hydrocortisone)
“Hapten-Hypersensitivity”
Immune Hemolytic Anemia
Signs of _________:
Jaundice - unconjugated bili
(Icterus)
Splenomegaly
Hemolytic Anemia
Signs of \_\_\_\_\_\_\_: anemia hemoglobinuria fatigue abd pain thrombosis
Paroxysmal nocturnal hemoglobinuria
Evaluation of _______:
Bone marrow aspirate showing abnormal increase in erythrocyte stem cells (erythroid hyperplasia)
Hemolytic Anemia
Lab Findings for \_\_\_\_\_\_\_: Low CBC High Hgb/Hct High reticulocytes Normal to High MCV
Hemolytic Anemia
Cause of ______:
Dehydration
Relative Polycythemia
Dehydration leads to decreased fluid in blood which means less floating space 2 groups of hemoconcentration -high Hgb/Hct/ RBC -Disturbed fluid balances -Stress-induced
Relative Polycythemia
Abnormal regulation of multipotent hematopoietic stem cells that is associated with a gene mutation and neoplastic transformation of bone marrow stem cells & absolute increased RBC mass
Primary Absolute Polycythemia
Polycythemia Vera
Key Points of \_\_\_\_\_\_: Rare in ages <40 Men>Women Cause unknown No cure Increased risk for stroke/ MI /HTN
Primary Absolute Polycythemia
Polycythemia Vera
Lab Findings for \_\_\_\_\_\_\_: Absolute increase in RBC mass leukocytosis (increased WBC) thrombocytosis (increased plt) increased uric acid (due to excess proliferation) normal O2 sat
Primary Absolute Polycythemia
Polycythemia Vera
Clinical Manifestations of \_\_\_\_\_\_\_\_: s/sx are all d/t increased blood viscosity • SOB • Dizziness • Red-colored face • Bluish extremities
Primary Absolute Polycythemia
Polycythemia Vera
Acute, self-limiting viral infection of B lymphocytes usually caused by Epstein Barr Virus (EBV) (~85% of cases)
Infectious Mononucleosis
Viral Causes of \_\_\_\_\_\_: Epstein Barr cytomegaly adenovirus HIV Hep A Influenza A & B Rubella
Infectious Mononucleosis
Bacterial Causes of _______:
Toxoplasmosis and Diphtheria
Infectious Mononucleosis
Bacterial Causes of _______:
Toxoplasmosis and Diphtheria
Infectious Mononucleosis
- Virus enters oropharynx, nasopharynx, or salivary epithelial cells & spreads to lymphoid tissue & B cells
- Virus causes widespread infxn of B lymphocytes that have receptors for the EBV
Meanwhile, the unaffected B lymphocytes produce IgG, IgM, & IgA against the virus
Cell-mediated response is in the form of cytotoxic T cells & cytokines that directly attack the EBV infected cells
This immune response produces cellular proliferation in the lymphoid tissue–specifically nodes, tonsils, spleen, & liver.
Patho of Infectious Mononucleosis
Labs for ______:
CBC (Differential with at least 50% lymphocytes and 10% atypical lymphocytes- classic triad, high leukocytes)
Monospot (qualitative test for heterophilic antibodies which increase as the illness progresses)
EBV specific antibodies
positive IgM antibodies (may not appear for 7-10 days)
Infectious Mononucleosis
Clinical Manifestations of \_\_\_\_\_\_\_\_: Sore throat Sore, Inflamed tonsils Exudate on tonsils (grey, thick) Fatigue (can last up to 2 months) Malaise Arthralgia ***Classic triad of symptoms: Fever, pharyngitis, and lymphadenopathy of the cervical lymph nodes (lasts 7-20 days)
Infectious Mononucleosis
incubation of Infectious Mononucleosis
30-50 days
prodomal phase of Infectious Mononucleosis with sx of fever, arthralgia, malaise
3-5 days
Adults 40 and older with mononucleosis are more likely to have infection from _______ or _________
cytomegaly virus or bacterial
Mononucleosis is more common in ages ______with ______/1000 cases per year
15-35
6-8
State of hypercoagulability which increases risk of thrombosis
thrombophilia
type of thrombophilia that results from defects in proteins that are involved in hemostasis
Inherited conditions (mostly autosomal dominnt) that increase risk for thrombosis
Ex: Factor V Leiden
Primary (hereditary)
type of thrombophilia that is caused by condition/disease that promotes venous stasis or changes in coagulation factors
Ex: Pregnancy
Secondary (acquired)
Genetic disease that is the most common hereditary thrombophilia
Factor V Lieden
Key Points of ________:
- Increases the risk of blood clots
- Alters clotting factor V
- Protein C cannot be degraded
- Hormonal birth control increases risk even without this factor – so women are screened
Factor V Lieden
Labs for _____:
Protein C
Genetic Testing
Factor V Lieden
_______ increases risk for ischemic stroke, DVT, & MI
Factor V Lieden
30% of patients w/ DVT or PE have ______
Factor V Lieden
Lab Findings for ______ & ______:
Prolonged PTT
Normal Platelets and INR
Hemophilia and Von Willebrand Disease
Lab Findings for ______:
Platelet Count <150,000
Normal PT/PTT/INR
Immune Thrombocytopenia Purpura (ITP)
most common blood disorder in children with the highest Incidence between 6mo – 2yrs old that is caused by ingesting too much cow’s milk which has a heat labile protein that casues inflammation and chronic intestinal blood loss
Iron Deficiency Anemia
Clinical Manifestations of _______:
Fatigue, weakness, dizziness, SOB, Tachycardia, HA, Leg cramps, Pale skin
Hemolytic Disease of the NB
Labs for \_\_\_\_\_\_\_: -Microcytic RBCs -Low MCV, MCH and MCHC -Hemoglobin electrophoresis (may be used to determine type of abnormal hemoglobin) Unconjugated bilirubin
Hemolytic Disease of the NB
Lab that tests for antibodies that stick to RBCs and cause hemolysis
Coombs
lab test used to detect antibodies that are stuck to the surface of RBC and cause hemolysis and anemia
-Positive test indicates that these antibodies are present
Direct Coombs
lab test that detects free-flowing antibodies against certain RBC
- Most often done to see if there is a potential transfusion reaction
- Positive: there are antibodies present and blood crossmatch is incompatible
Indirect Coombs
an unstable and insoluble form of Hgb resulting from defective Hgb synthesis in Sickle Cell Disease
HBs
genetic defect in which valine replaces glutaminic acid in Hgb
Sickle Cell Disease
RBC with high levels of HBs are very sensitive to ________ so they fold or “sickle”
low O2 states
Sickling is reversible except when _____ are present in very high percentage
HBs
In ________, anemia is caused by rapid death of defective RBCs that have only 16-20 day lifespan
Sickle Cell Disease
Sickle Cell Disease is _______ ________ Disorder (must have a defective gene from both parents to show phenotype)
Autosomal Recessive
This occurs when a child inherits Hb S from one parent and normal hemoglobin (Hb A) from the other and this heterozygous carrier rarely has symptoms
Sickle Cell Trait
Symptoms of Hgb S do not appear until age ______ when fetal Hgb is replaced by Hgb produced by the infant
6 months
Clinical Manifestations of ______:
• Recurrent pain
• Disability
• Organ damage
• Increased infections (most common cause of death)
• Early death (people are now living into 40-50s)
Sickle Cell Disease
Group of inherited disorders caused by variant or missing genes that affect how the body makes Hgb (microcytic hemolytic anemia)
Thalassemias
The type of _______ (alpha or beta) depends on the type of Hgb that is low or missing
Thalassemias
Inhereited Severity of \_\_\_\_\_\_\_\_\_: Carrier Intermedia Trait/Minor: heterozygous inheritance may not have sx Major: homozygous inheritance- may require blood transfusions
Thalassemias
Thalassemias is a ________ ________ disorder
autosomal recessive
Hemolysis of reticulocytes leads to elevated iron and indirect bilirubin
patho of Thalassemias
Type of hemophilia: Factor VIII deficiency
• Most common inherited coagulation disorder
that leads to excessive bleeding
• X-linked (boys only)
• Often discovered during circumcision
Type A (classic)
Type of hemophilia: Factor IX deficiency
• X-linked
Type B (Christmas disease)
type of hemophilia: Factor XI deficiency
• Autosomal recessive
• Occurs in boys and girls
• Less severe
Type C
Autosomal dominant (most) disorder affecting Factor VIII deficiency (key clotting protein) and platelet dysfunction
• Most common bleeding disorder for both men and women
• Carried on chromosome 12
Von Willebrand Disease
protein that binds factor VIII and platelets and BV walls to create platelet plugs.
Von Willebrand protein
Clinical Manifestations of ______:
Hematoma formation
Persistent bleeding from minor laceration
Von Willebrand Disease
Lab Findings of ________:
Prolonged aPTT
Normal platelets and INR
Von Willebrand Disease
Antiplatelet antibodies bind to platelet plasma membranes causing platelet sequestration & destruction resulting in low platelet count & increased risk of hemorrhage usually occuring after a viral infection→ large amount of antigen in blood → formation of immune complexes → bind to platelets → platelet destruction
Immune Thrombocytopenia Purpura in Children
Key Points of \_\_\_\_\_\_\_: • Type II hypersensitivity • Resolves when antigen is removed • Persistent cases can last 3-12 months • Autoimmune or primary thrombocytopenic purpura
Immune Thrombocytopenia Purpura in Children
Clinical Manifestations of \_\_\_\_\_\_\_\_\_: Bruising generalized petechial rash asymmetrical bleeding spontaneous bleeding (Platelet count <15,000) resulting in • Petechiae • Ecchymosis • Purpura
Immune Thrombocytopenia Purpura in Children
Lab Findings for _______:
Platelet count <150,000
Normal PT/ INR/PTT
Immune Thrombocytopenia Purpura in Children
caused by changes in expressions of the genes involved in cell division
Cancer
ONE CELL can generate widespread metastatic disease
monoclonal origin of cancer
NOT inherited from one human generation to another • UNLESS mutation is present in a gene that regulates cell division in a germline cell, then it CAN be inherited and this mutation in germline cells can significantly increase the risk
Cancer
_______ develops as a results of 3 interacting factors:
• Environmental exposure to carcinogens
• Health of immune function
• Genetic predisposition
Cancer
This germline mutation is present in one BRCA 1 allele throughout all of the person’s cells. The cells have essentially already gone through half of initiation at conception and require only one additional allele mutation followed by promotion for the malignancy to occur. While the person carries genetic changes which could lead to development of cancer, they have not inherited the cancer itself – it requires further mutation/changes to develop into cancer.
BRCA 1 suppressor gene mutation
Characteristics of \_\_\_\_\_\_\_ Tumor: • Grow slowly • Well-defined capsule • Not invasive • Well-differentiated • Low mitotic index • DO NOT metastasize
Benign
Characteristics of \_\_\_\_\_\_ Tumor: • Grow Rapidly • Not encapsulated • Invasive • Poorly differentiated • High Miotic Index • Can spread distally (Metastasis)
Malignant
Stage of Metastatic Disease
• A carcinogen causes genetic mutation that activates proto oncogenes which inactivates tumor suppressor genes.
• The mutation is not evident until PROLIFERATION
• Proliferation is required for cancer development!
• Initiation is irreversible
• It only takes ONE transformed cell to start the cancer process
Initiation
Stage of Metastatic Disease:
• Occurs when mutant cells begin to proliferate through the enhancement of the growth of the initiated cell.
• Promoters: infection, hormones, nutritional factors, cigarette smoke, etc.
• Cancer synthesize telomerase when they become malignant. This process of synthetization allows the cell to have immortality as it continually regenerates the telomeres.
• Cells are not immortal and can divide only a certain number of times.
• Telomeres are protective caps on each chromosome and are held in place by telomerase
• Telomeres become smaller and smaller with each cell division
• Cancer cell telomeres do not become smaller with cell division and telomeres can be restored, leading to continued division and immortality.
• Cancer cells are P-53 deficient which allows the cell to escape apoptosis, though DNA is grossly abnormal.
Promotion
Stage of Metastatic Disease:
• Continued genetic changes that occur over time- gives survival changes to cancer cells (the cell begins to display malignant behaviors)
• Some cells will have growth advantage and proliferate more readily.
• Some cells are able to develop a separate blood supply through tumor angiogenesis factor (TAF)
Progression
Stage of Metastatic Disease:
• Loss of differentiated function, cell becomes more efficient in cell division → METASTASIS
• Metastasis occurs when cancer cells escape the tissue of origin and initiate colonies of cancer at distant sites via blood and lymph circulation.
Metastasis
Genes associated w/ initiation of cancerous behavior in a cell that are promitotic and induce cells to divide and proliferate ***Mutations occurs less frequently,
Oncogenes
the loss of oncogene sensitivity to suppressor gene regulation leads to….
oncogene overexpression
normal cellular gene that is growth promoting.
***When this is erroneously activated, it becomes an oncogene and promotes cancer
Proto-oncogenes
these genes regulate a group of growth-promoting genes and suppress tumor formation
• They inhibit mitosis and trigger apoptosis
• Mutation and under-expression of this gene is associated with cancer development
Tumor Suppressing Gene
Examples of _______:
P-53- suppresses tumor formation
RB Tumor suppressor - this is inactivated in occurrences of Retinoblastoma
BRCA 1 - Inactivated in occurrences of Breast and Ovarian Cancer
BRCA 2- Inactivated in occurrences of ovarian, breast, and prostate carcinomas
Tumor Suppressing Genes
Mutations in _________ (even if only in one allele), reduces the ability of the suppressor gene products to inhibit the activity of the promitotic oncogenes
Tumor Suppressing Genes
Mutations in suppressor genes alleles or DNA repair genes cause most _________
cancer
- Occurs usually as a result of environmental exposure or unknown factors
- No observable pattern of inheritance
- Mutations of carcinogenesis disrupt regulation of cell division (usually somatic cells)
- Not present in higher-than-expected levels within three family generations
Sporadic Cancer
- Occurs at a higher-than-expected frequency within a family
- Does not demonstrate observable pattern of inheritance
- Family may have higher-than-expected incidence of several cancer types
- Those who develop cancer are older (usually over 60)
Familial Cancer
• Cancer that occurs with an observable autosomal dominant pattern within a family
• Diagnosis at much younger-than-expected ages
• Caused by germline mutations in suppressor genes
• RISK is inherited - NOT the actual cancer
*****Risk is greatly increased, but NOT absolute. (AGING, IMMUNOCOMPROMISED ALSO INCREASES PERSONAL RISK)
Inherited Cancer
immature form of RBC
reticulyte
disruption of dna synthesis of blast cells in bone marrow produces megaloblasts (large abnormally shaped RBC with normal Hgb)
macrocytic normochromic anemias
folate + B12 deficiency anemias
gastrectomy makes you think…
pernicious anemia
What is it that causes parasthesis of the fingers and hands in B12 deficiency?
demyelination in the spinal cord
What does B12 + folate deficiency do in the bone marrow that lead to macrocytic anemia?
DNA synthesis of the RBC disrupted
What symptom is seen in all anemias?
fatigue
spoon-shaped nails
koilynichia
type of Hgb that is present in newborns but slowly fades away with age
Hgb F
normal type of Hgb
Hgb A
type of Hgb present in sickle cell disease
Hgb S
myeloproliferative disorder, increase in RBCs resulting in an increase in blood viscosity leading to clinical symptoms such as HTN
polycythemia
most common type of polycythemia that is due to chronic hypoxemia
increased erythopoitein production
increase in RBC w/o increase in WBC or platelets
*seen in individuals w/ lower O2 serum concentration
(high altitude or smokers)
secondary polycythemia
condition that usually occurs after a viral infection that leads to a large amount of antigen in the blood that forms immune complexes with circulating antibodies that bind to receptors on platelets and cause platelet destruction
Autoimmune or Primary Thrombocytopenic Purpura
Primary Thrombocytopenic Purpura is a Type ___ Hypersensitivity
2
Clinical Manifestations of ________:
Bruising, generalized petechial rash, asymmetrical bleeding
Autoimmune or Primary Thrombocytopenic Purpura
Lab Findings for ______:
o Low platelet count
o Increased bleeding time
o Normal PT, PTT, & INR
Autoimmune or Primary Thrombocytopenic Purpura
type of polycythemia that is due to dehydration because decreased fluid within bloodstream it looks like there are more RBCs but really you just have less floating space
Relative Polycythemia
First test to order when patient presents with fatigue
CBC
increase in reticulocyte count tells us what?
bone marrow is responding to a decrease
increase related to treatment with iron
MCV tells us what about RBC?
size
MCH tells us what?
weight/mass of Hgb per RBC
MCHC tells us what?
Hgb concentration of average RBC?
bleeding time tells us what?
how long it takes to clots?
bleeding time is testing which RBC?
platelets
Hgb electrophoresis
differentiates between Hgb A, S or F
Which test is most sensitive for detecting clotting factor defects?
aPTT
aPTT and PTT tests screen for what?
clotting factor defects
D-dimer is a screening test for what?
blood clots
Mutations of Rb (tumor suppressing gene) are inherited via ____?
autosomal dominant or sporadic
How does chronic inflammation cause cancer?
cell mutation due to inflammatory process of releasing O2
tumor markers are found where?
blood, spinal fluid, urine
ca125 screening is for?
ovarian cancer
chromosome instability may result in the over expression of _______
oncogenes
pernicious anemia caused by autoimmune destruction of parietal cells that make intrinsic factor
megaloblastic anemia
macrocytic anemias
pernicious anemia
B12 deficiency anemia
folate deficiency anemia
microcytic anemias
iron deficiency anemia
thalassemia (inherited)
normocytic anemias
hemolytic anemia
post-hemorrhagic anemia
lymphocyte function ______ with age (in particular cellular immunity)
decreases
BRCA1 gene is associated which cancers?
breast, ovarian, prostrate
type of Hgb seen with beta-thalassemia
HgbA2
folate is stored in the _____
liver
folate absorption occurs in the ______
small intestine
most common form of autoimmune hemolytic anemia
warm antibody
Causes of \_\_\_\_\_\_\_: hypoxemia **most common increased plasma osmolality/volume low temperature decreased pH dehydration
Sickling
these negatively regulate proliferation
tumor suppressing genes
Hep B, Hep C, Epstein Barr & HPV have all been linked to…
cancer development
genes that encode proteins to repair DNA whose loss of function results in increased mutation rates and cancer rates
caretaker genes
test used to detect antibodies that are stuck to the surface of RBCs, These antibodies sometimes destroy RBCs and cause anemia.
Direct Coombs
______ direct coombs test means there are antibodies that act against the RBCs
positive
test that looks for free flowing antibodies against certain RBCs -most often used to see if there is a blood transfusion reaction
Indirect Coombs
______ indirect coombs test means there are free flowing antibodies that will act against RBCs that the body views as foreign= incompatible blood match
positive
