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NUR 305 - Immunity and Oncology

Terms in this set (90)

bone marrow
produces all the different cells
in adults include vertebrae, ribs, sternum, and ilia
kidney
secretes Erythropoietin when hypoxia detected
erythropoietin (hormone) that stimulates red blood cell production
liver
produces prothrombin and other clotting factors
stores extra iron as ferritin
spleen
destroys red blood cells that are old or abnormal; "graveyard of RBCs"
breaks down hemoglobin
stores platelets
filters antigens
rich in lymphoid tissue (contains B and T lymphocytes)
lymphatic system
lymphatic vessels
lymph nodes
-lymphadenopathy: enlargement of lymph node in response to proliferation of lymphocytes
thymus (T lymphocyte maturation)
bone marrow (B lymphocyte maturation)
complete blood count (CBC)
standard blood test
blood is examined in a smear
different types of cells are counted
stains differentiate WBCs
measures the levels of:
-RBCs
-WBCs
-platelets
-hemoglobin (Hgb)
-hematocrit (Hct)
-other differentials in the RBCs and WBCs
CBC with differential
tells the different levels of each WBC count
overactive immune systems cause
autoimmune disease
allergies
hypersensitivity reactions
immune system protects us against
external threats (microbial)
internal threats (e.g. precancerous cells)
performs maintenance (cleanup of dead or damaged cells)
endothelial cell
blood vessel lining
selective permeability barrier to inflammatory stimuli
regulatory role with WBC, inflammatory mediators
repair process for vessels
platelets
release inflammatory mediators when activated that influence endothelial cells
blood clotting
neutrophils
most numerous
first responders at the site of inflammation and infection
scavenge and engulf bacteria/debris
short life span (24-48 hrs)
not specific
high count means early in infection, low means the infection has been occurring longer
eosinophils
quick response to inflammation site; destroy parasites
release chemical mediators in allergic reactions
long life span
basophils and mast cells
prominent in allergic reactions
responds to IgE to release histamine and vasoactive agents
mast cells
do not develop until lodged in tissues
activate other WBCs
mature form of basophils
monocytes
mature into macrophages
produce vasoactive mediators involved with inflammation
macrophages
engulf and kill bacteria
longer life span allows them to resolve inflammatory process and promote healing in tissues
pacman of the immune system: restore health of tissue after inflammation
lymphocytes
B and T types
work with macrophages to promote inflammation, including chronic
respond to antigens and endow long-term immunity
plasma cells
plasma cells develop from activated B cells
leukocytosis
high WBC count- elevation in WBC count > 10 x109/L
due to inflammation, stress, infection, cancer, and bone marrow disorders
CBC with differential
-increase in one WBC helps identify possible cause of leukocytosis
-most common rise is neutrophils due to infection, inflammation, or cancer
cytosis
high cell count
thrombocytosis
abnormally high platelet count
leukopenia
decrease in WBC in blood (< 4 x109/L)
caused by bone marrow deficiencies: chemotherapy, radiation, leukemia/ lymphoma, splenomegaly, autoimmune disorders, medication side effect
increases risks for infection, decreases signs of infection, diminishes healing
fever is always consider a symptom of infection
neutropenia
low neutrophil count- virtual absence of neutrophils (Congenital and Acquired)
aplastic anemia
not making any myeloid cells
deficiencies in all myeloid cells affected (anemia, thrombocytopenia, and agranulocytosis)
innate immunity
born with this
present even before an infection encountered
natural anatomical barriers- physical and chemical
phagocytic neutrophils, macrophages, natural killer (NK) cells, complement system
recognize and kill infectious agents
cytokines
chemical messengers
promote inflammation and attract leukocytes
interferons
destroy viruses
proteins released from virus-infected cells and bind to nearby uninfected cells
-the uninfected cells release an enzyme that prevents viral replication
-when the virus infects the cells, replication of the virus is prevented
adaptive immunity
body must learn this
distinguishes among different microbes and remembers pathogens
recognizes and responds to antigens
-histocompatibility antigens distinguish self from non-self
examples of antigens
-infectious: viruses, bacteria, fungi, parasites
-noninfectious: pollens, foods, bee venom, drugs, vaccines, transfusions and transplanted tissues
cell-mediated immunity
T Lymphocytes:
-helper (CD4)- don't destroy, but support process
-cytotoxic (CD8)- destroy the invader
-memory T Cell- how we learn the response
Antigen-Presenting Cells (APC):
◦Macrophages
◦Dendritic cells
Antigen provokes APC
-APC processes antigen and displays it on cell membrane
-CD8 attack the antigen
-CD4 yield cytokines to promote inflammation
-Complement systems promotes inflammation
humoral immunity
B lymphocytes
-plasma Cells
-memory B Cells
Primary Phase
-naïve B cell stimulated by an antigen to mature into plasma cell
-CD4 cells attack antigens to blunt effect of pathogen
-plasma cells secrete Igs
-Igs bind to and inactive antigen
-memory cells created to remember antigen for future exposures
Secondary Phase: Faster response to antigens by Igs
-antibodies or immunoglobulins (Igs): serum glycoproteins produced by plasma cells in response to an antigen challenge
-include IgG, IgA, IgM, IgE, and IgD
IgG
most abundant
displays antiviral, antitoxin, and antibacterial properties
only ig that crosses and thus responsible for protection of newborn
activates complement and binds to macrophages
prominent in the secondary immune response
IgA
predominant lg in body secretions, such as saliva, nasal, and respiratory secretions, and breast milk
protects mucous membranes
IgM
forms the natural antibodies such as those for ABO blood antigens
prominent in early immune responses
activates complement
IgD
found on b lymphocytes
needed for maturation of B cells
IgE
binds to mast cells and basophils
involved in parasitic infections and allergic and hypersensitivity reactions
active immunity
long lasting but takes a few days to become effective
body's immune system engages in responding to antigen
active natural - contact with antigen thru clinical infection (chicken pox, measles, mumps)
active artificial - immunization with live or killed vaccines
passive immunity
short lasting
fully formed antibodies provided from external source
passive natural - transplacental and /or breast milk transfer from mother to child
passive artificial - injection of serum from immune human (ex. injection of human gamma-globulin, rabies, tetanus, snake bite)
hypersensitivity
inflated immune response to a foreign substance
autoimmune
mistakes self as non-self
penetration
disruption in integrity of the surface barrier
direct contact
transmission of infected tissues or secretions to exposed, intact mucous membranes- common entry for STIs
ingestion
oral cavity and GI tract is a more efficient means of entry
agent must survive the low pH and enzymes of gastric sections, peristalsis of intestines, and normal flora
inhalation
respiratory tract has protective mechanisms in place- cilia and mucus, humidification, coughing, antibodies and enzymes in secretions; if these are overcome or impaired (smoking, CF, emphysema) a person can become ill
incidence
new cases
prevalence
number of cases overall
incubation period of infection
exposure then replication but hasn't activated immune system
microorganism begins active replication without producing identifiable symptoms
prodromal stage of infection
initial appearance of symptoms (typically vague)
acute stage of infection
host experiences full infectious disease with rapid proliferation of the pathogen
immune system and inflammation reaction in full force
convalescent stage of infection
infection contained and progressively eliminated
resolution of symptoms begins
immune system releases antibodies and wins
resolution phase of infection
elimination of the pathogen without residual signs or symptoms
body is back to normal
Immediate Hypersensitivity: Type I
IgE mediated (IgE antibody)
Allergic reactions to allergens
Produces an immediate response
Rapid reaction in which IgE binds to mast cells and combine with antigen; histamine released; eosinophils attracted and release more inflammatory mediators
Local response:
-hives, nasal or conjunctival discharge, bronchial asthma, allergic gastroenteritis
Examples:
-hay fever, food allergies, and anaphylaxis
Cytotoxic Hypersensitivity: Type II
Antibody-mediated reaction
IgG or IgM type antibodies that react to foreign tissue of cells
Lysis of blood cells occurs because of the activation of the complement
Examples:
-Blood transfusion reaction and erythroblastosis fetalis (maternity when mom and baby's blood types are not compatible)
Immune Complex Hypersensitivity: Type III
Circulating antigen-antibody complexes accumulate and are deposited in the tissue
Triggers the complement system and inflammation
Damages different organs
Example:
-Autoimmune conditions (e.g. systemic lupus erythematosus)
Delayed Hypersensitivity: Type IV
Cell-mediated rather than antibody-mediated involving the T cells
T lymphocytes respond to antigens days after initial exposure
Examples:
-tuberculin skin testing, transplant reactions, and contact dermatitis
autoimmune disorders
Immune system loses the ability to recognize self
Defenses are directed against host
Known characteristics:
-Genetics play a role
-More prevalent in females
-Onset = stressor, either physical or psychological
-Often have periods of exacerbation and remission
immunodeficiency
Diminished or absent immune response
Renders the person susceptible to disease normally prevented by the immune system
Opportunistic infections (fungal, certain bacteria and viruses)
May be acute or chronic
Classifications:
-Primary (genetic)- specific thing in body that causes this
-Secondary (acquired)- something else going on, because of that there is another disease- first infection wore out immune system
Epstein Barr Virus
Infectious mononucleosis
Virus binds to and infects oropharynx
Virus causes proliferation of B lymphocytes and lymphadenopathy
Transferred through oral secretions
Manifests with bilateral lymphadenopathy, pharyngitis, fatigue, headache, fever, chills, nausea/vomiting, abdominal pain
Symptoms last 4 weeks, but recovery may take up to 6 months
Dormant phase versus acute infection
lymphadenopathy
swollen lymph nodes
pharyngitis
inflammation of the pharynx
HIV
parasitic retrovirus that infects CD4 cells
Two primary types:
-Type I is the most common strain
-Type 2 is more common in West Africa; progresses to disease more slowly
Risk Factors:
-unprotected sexual activity
-anal intercourse
-IV drug abuse
-frequent blood transfusions
High Risk Groups:
-Men who have sex with men
-African Americans
-Hispanics
In the US, rates rising among women and African Americans
AIDS progression
Asymptomatic phase:
-virus is reproducing, usually for several years
Infections begin as the viral number rises, destroying the CD4
Progression takes three forms:
-immunodeficiency
-autoimmunity
-neurological dysfunction
Diagnosis:
-Gold standard diagnosis is HIV RNA assay for acute infection
-After seroconversion (2 weeks-6 months) ELISA test and Western Blot test used
HIV and AIDS Classification System
Two systems, one based on lab findings and the other laboratory findings for CD4 T-cell counts
! normal 700-1200 cells/microL!
- Category 1: >500 cells/microL
-Category 2: 200-499 cells/microL
-Category 3: <200 cells/microL
Clinical; based on clinical manifestations:
-Category A: asymptomatic
-Category B: some less serious manifestations of immune deficiency-fever, lymphadenopathy, arthralgias, headache, pharyngitis, fatigue, GI symptoms
-Category C: AIDS (Acquired Immune Deficiency Syndrome) defining illnesses present and high risk for opportunistic infections
cyclins
promote cell division
supressor gene
limit cell division
contact inhibition
stops further rounds of cell division when surrounded and touched by other cells
benign tumor
overgrowth of tissue
characteristics:
-Specific Morphology
-A Smaller Nuclear-to-Cytoplasmic Ratio
-Specific Differentiated Functions
-Tight Adherence
-No Migration
-Orderly Growth
-Normal Chromosomes
malignant tumor
characteristics:
-Anaplasia
-A Larger Nuclear-to-Cytoplasmic Ratio
-No Specific Functions
-Loose Adherence
-Migration
-Contact Inhibition Does Not Occur
-Rapid or Continuous Cell Division
-Abnormal Chromosomes (Aneuploidy)
cancer - stage 1
found tumor
tumor limited to the tissue of origin; localized tumor growth
cancer - stage 2
tumor vascularization
trigger production of blood vessels
tumor has its own supply of blood
cancer - stage 3
cancer cells have broken off from the main tumor
enzymes on the surface of cells make holes in the blood vessels, allowing cancer cells to enter blood vessels and travel around the body
cancer - stage 4
cancer clumps up in blood vessels and invade new tissue areas
if the new tissues have the right conditions to support continued growth of cancel cells, new tumors (metastatic tumors) will form at this site
Warning Signs of Cancer
Changes in bowel or bladder habits
A sore that does not heal
Unusual bleeding or discharge
Thickening or lump in the breast or elsewhere
Indigestion or difficulty swallowing
Obvious change in a wart or mole
Nagging cough or hoarseness
White patches inside mouth or on tongue
Unexplained fever
Unexplained tiredness / Fatigue
Weight less of 10 pounds or more- cancer cells use a lot of energy
Persistent pain or discomfort
leukemia
Abnormal proliferation of precursor stems cells for WBCs
lymphoma
Abnormal proliferation of B or T lymphocytes in lymph nodes or lymphoid tissue (solid tumors)
-Most common type of blood cancer
3 interacting factors influence cancer development
Exposure to carcinogens:
-Chemicals, Drugs,
-Chemotherapy/Radiation
-Some viruses
Genetic predisposition:
-Tumor Suppressor Genes: restrain cell growth; mutation or defect leads to cancer
-Oncogenes: mutation of proto-oncogenes; stimulates uncontrolled cell proliferation
Immune function:
-Decreases with age, increasing risk for cancer
diagnosis of cancer
Screenings
Physical Assessment
CBC with differential
Bone marrow aspiration and analysis
Lymph node biospies
FISH test (assess chromosome defects)
Flow cytometry (staging and prognosis for leukemia)
Classification and Staging:
-Tumor
-Nodes
-Metastasis
Acute Lymphocytic Leukemia
Most common in children
Quickly symptomatic
23% childhood cancers
Pre-B or Pre-T lymphocytes do not function or mature
-Lymphoblasts ("Blasts")
No known cause
Lymph nodes, CNS, kidneys, and testicles can be infiltrated with lymphoblasts
T-cell ALL has worse prognosis
Acute Lymphocytic Leukemia Manifestations
Non-specific at first (like a virus): fever, chills, night sweats, flu-like symptoms
May have frequent infections (loss of healthy WBC)
May have fatigue, dyspnea, and pallor (loss of healthy RBC)
Unexplained bruising/bleeding (loss of healthy platelets)
Enlarged lymph node or spleen is often first sign
May have bone pain
Headaches (CNS involvement)
High lymphoblast count in bone marrow
Chronic Lymphocytic Leukemia
Most common leukemia in US
Malignancy of B-Lymphs
Common in older adults (average age of diagnosis is 70 years old)
More common in males, advanced age, Caucasian, family history of hematologic cancer, exposure to toxins
Precursor B cells failed to mature and have minimal function- produce abnormal Ig
Chronic Lymphocytic Leukemia Manifestations
Unremarkable history at first
Enlarged, painless lymph node
Fatigue, fever, night sweats, weight loss
Pain in upper left abdomen (spleen enlargement)
Frequent infection
May identify by abnormally high WBC count on routine blood work
Acute Myelogenous Leukemia
Proliferation of undifferentiated myeloid (blast) cells in bone marrow
Can invade blood, tissues, spleen, liver, skin (rash), lungs
Risk factors: previous chemo and radiation
Acute Myelogenous Leukemia Manifestations
Non-specific at first (like a virus): fever, chills, night sweats, flu-like symptoms
May have frequent infections (lack of healthy WBC)
May have fatigue, dyspnea, and pallor (lack of RBC)
Unexplained bruising/bleeding (lack of healthy platelets)
High myeloid blast count in bone marrow
Chronic Myelogenous Leukemia
Overproduction of mature myeloid cells in bone marrow
Common in older adults (Median age diagnosis is 50 years)
95% have Philadelphia chromosome
15-20% of all leukemia
Chronic Myelogenous Leukemia Manifestations
3 Phases:
- phase 1: Chronic phase (asymptomatic): neutrophils lose differentiation
- phase 2: Accelerated phase: neutrophils more undifferentiated and unable to function
- phase 3: Blast Crisis (Terminal) Phase (evolution to acute leukemia): no differentiation
Signs and Symptoms of Blast Crisis:
First sign is fatigue
May have frequent infections (lack of healthy WBC)
May have fatigue, dyspnea, and pallor (lack of RBC)
Unexplained bruising/bleeding (lack of healthy platelets)
Fever, weakness, night sweats
Bone pain
Splenomegaly, hepatomegaly, respiratory distress
Malignant Lymphomas
First sign is painless, enlarged lymph node in neck, under arm, or in groin
Other symptoms: splenomegaly, hepatomegaly, fever, chills, weight loss, night sweats, lack of energy, itching
Symptoms are similar- diagnosed by biopsy
Non-Hodgkin's Lymphoma
-83% lymphoma cases
-Most common in middle age and older adults; more males than females
-Malignant transformation of either T or B lymphocytes or NK cells
-May cause lymphatic blockage (swelling in arm or leg); nerve impairment (pain, numbness, tingling); stomach (fullness)
-Staging: I through IV
Hodgkin's Lymphoma
-17% lymphomas
-Most common in 15-20 years and 50 years or older
-Abnormal B lymphocyte (Reed-Sternberg Cell)
-Typically originate in a single lymph node and then spreads to contiguous nodes
-Associated with pharyngeal edema, sore throat, dysphagia
-Staging is more critical
- More aggressive and can impair airway
-Starts in neck and chest area
-REED-STERNBERG CELLS
Multiple Myeloma
Proliferation of abnormal plasma cells (matured B lymphocytes) in bone marrow
Synthesis of abnormal Igs
Incurable
High incidence in men and African Americans
Generalized disorder leading to bone destruction (increased osteoclasts), bone marrow failure, renal failure (hypercalcemia and nephropathy), neurological complications, and amyloidosis (build up of amyloid protein in organs)
Bone pain (in back) is common complaint
Weakness, pallor, fatigue (due to anemia), infection (due to loss of antibody-mediated immunity)
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