Hematology/Neoplasms Flashcards by Kristin Godsey

a test to measure Hgb S

hemoglobin electrophoresis

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low hemoglobin and hematocrit, small red blood cells, and an increased total iron binding capacity are all signs of…

iron deficiency anemia

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lab test used to to evaluate red blood cell size

mean corpuscular volume

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best laboratory test for detecting a clotting factor defect

aPTT

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beta thalassemia minor, the genetic defect is in the ________

Hemoglobin

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Cancers arise in cells that have alterations in the ______

genes

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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)

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For full-term neonates: these are comparable to counts in adults and remain so throughout infancy and childhood

platelets

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normal erythrocyte life span in full-term infants

60-80 days

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normal erythrocyte life span in pre-term infants

20-30 days

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erythrocytes have many ______ in full-term infants

reticulytes

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normal erythrocyte life span in children/adolescents/adults

120 days

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aging causes erythrocytes to ________ while maintaining normal lifespan

replenish more slowly

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Causes of \_\_\_\_\_\_\_ in Aging
Fe++ depletion
Decreased total serum Fe++
Decreased Fe++ binding capacity
Decreased intestinal Fe++ absorption

erythrocyte replacement slowing

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Signs of \_\_\_\_\_\_\_ in the hematological system:
Platelet adhesiveness increases
Lymphocyte function decreases
T-cell function declines
Humoral system less responsive

Aging

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large cells with normal Hgb

macrocytic normochromic anemias

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Risk Factors for \_\_\_\_\_\_\_\_:
Dietary deficiency
alcoholism
cirrhosis
malabsorption
increased requirement state (pregnancy)

folate anemia

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low maternal folate leads to ______

neural tube defects

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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

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Folate deficiency leads to abnormal _______ in RBC (as in B12 deficiency)

DNA synthesis

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Both ________ have defective DNA synthesis in the bone marrow

folate and B12 anemia

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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 &amp; tongue (burning mouth syndrome)
dysphagia
flatulence
watery diarrhea
***Generally don’t see neurologic or psychiatric manifestations**

Folate Anemia

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condition with high MCV: the RBC’s are large w/ normal Hgb, MCHC, MCH

macrocytic anemia

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a measure of the concentration of haemoglobin in a given volume of packed red blood cel

mean corpuscular hemoglobin concentration (MCHC)

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average mass of hemoglobin per red blood cell in a sample of blood

mean corpuscular hemoglobin (MCH)

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Autoimmune disorder that causes destruction of the parietal cells in the stomach with complete loss of intrinsic factor

Pernicious (B12 Deficiency) Anemia

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enzyme that is necessary for the absorption of B12

intrinsic factor

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Risk Factors for \_\_\_\_\_\_:
Alcoholism
cirrhosis
bariatric surgery
 H. pylori
medications (H2 blockers, proton pump inhibitors)

Pernicious (B12 Deficiency) Anemia

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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

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_____ mostly affects older women (median age = 60)

Pernicious (B12 Deficiency) Anemia

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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

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methylmalonic acid is high in pernicious anemia because…

B12 is needed to break it down

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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

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small cell size with decreased Hgb

MCV, MCHC low

Microcytic Hypochromic Anemia

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Causes of \_\_\_\_\_\_\_:
Nutritional deficiency
blood loss (slow-GI bleed, fast-hemorrhage)
Less common: 
decreased GI absorption
pregnancy
renal failure

Iron Deficiency Anemia

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______ results in pale, small RBCs with lower than normal Hgb concentration

Iron Deficiency Anemia

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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

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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

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Normal cell size and Hgb

Normochromic/Normocytic Anemias

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anemia caused by accelerated destruction of RBCs in which Erythrocyte production is unable to keep up with destruction

Hemolytic Anemia

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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

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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

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type of hemolytic anemia that is due to an allergic rxn against foreign antigens: the drug (penicillin, cephalosporins, hydrocortisone)
“Hapten-Hypersensitivity”

Immune Hemolytic Anemia

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Signs of _________:
Jaundice - unconjugated bili
(Icterus)
Splenomegaly

Hemolytic Anemia

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Signs of \_\_\_\_\_\_\_:
anemia
hemoglobinuria
fatigue
abd pain
thrombosis

Paroxysmal nocturnal hemoglobinuria

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Evaluation of _______:

Bone marrow aspirate showing abnormal increase in erythrocyte stem cells (erythroid hyperplasia)

Hemolytic Anemia

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Lab Findings for \_\_\_\_\_\_\_:
Low CBC
High Hgb/Hct
High reticulocytes
Normal to High MCV

Hemolytic Anemia

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Cause of ______:

Dehydration

Relative Polycythemia

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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

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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

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Key Points of \_\_\_\_\_\_:
Rare in ages <40
Men>Women
Cause unknown
No cure
Increased risk for stroke/ MI /HTN

Primary Absolute Polycythemia

Polycythemia Vera

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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

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Clinical Manifestations of \_\_\_\_\_\_\_\_:
s/sx are all d/t increased blood viscosity
•	SOB 
•	Dizziness
•	Red-colored face
•	Bluish extremities

Primary Absolute Polycythemia

Polycythemia Vera

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Acute, self-limiting viral infection of B lymphocytes usually caused by Epstein Barr Virus (EBV) (~85% of cases)

Infectious Mononucleosis

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Viral Causes of \_\_\_\_\_\_:
Epstein Barr
cytomegaly
adenovirus
HIV
Hep A
Influenza A &amp; B
Rubella

Infectious Mononucleosis

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Bacterial Causes of _______:

Toxoplasmosis and Diphtheria

Infectious Mononucleosis

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Bacterial Causes of _______:

Toxoplasmosis and Diphtheria

Infectious Mononucleosis

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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

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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

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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

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incubation of Infectious Mononucleosis

30-50 days

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prodomal phase of Infectious Mononucleosis with sx of fever, arthralgia, malaise

3-5 days

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Adults 40 and older with mononucleosis are more likely to have infection from _______ or _________

cytomegaly virus or bacterial

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Mononucleosis is more common in ages ______with ______/1000 cases per year

15-35

6-8

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State of hypercoagulability which increases risk of thrombosis

thrombophilia

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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)

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type of thrombophilia that is caused by condition/disease that promotes venous stasis or changes in coagulation factors
 Ex: Pregnancy

Secondary (acquired)

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Genetic disease that is the most common hereditary thrombophilia

Factor V Lieden

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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

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Labs for _____:
Protein C
Genetic Testing

Factor V Lieden

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_______ 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

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

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Hematology/Neoplasms Flashcards

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