Term
|
Definition
| a substance/molecule that, when introduced into the body, triggers the production of an antibody by the immune system, which will then kill or neutralize the antigen that is recognized as a foreign and potentially harmful invader. |
|
|
Term
|
Definition
| a non-parasitic antigen capable of stimulating a type-I hypersensitivity reaction in atopic individuals |
|
|
Term
|
Definition
| a hypersensitivity disorder of the immune system. Allergic reactions occur to normally harmless environmental substances known as allergens; these reactions are acquired, predictable, and rapid. |
|
|
Term
|
Definition
| means it runs in the family |
|
|
Term
| What are mast cells? and where are they located? |
|
Definition
Mast Cells are large cells with granules in their cytoplasm, they contain a mixture of chemical mediators that act rapidly to make local blood vessels more permeable. Location: Mast cells are found in abundance in vascularized connective tissue just beneath body epithelial surfaces (submucosal tissues of GI and respiratory tracts, and skin) |
|
|
Term
|
Definition
| A chemical substance that facilitates and spreads inflammation. They are "Go-betweens" that facilitate communication between cells. Some are derived from cells and some are derived from plasma. |
|
|
Term
| What are the two types of mediators? |
|
Definition
Exogenous mediators - Chemotactic factors from bacteria that cause direct tissue injury Endogenous mediators - Are released from injured tissues and spread into uninjured areas, they are more numerous and more important than exogenous mediators. They are responsible for the spread of an acute inflammatory response following injury. |
|
|
Term
| What is the purpose of Antigen Presenting Cells? |
|
Definition
| Antigens must be properly proscessed by antigen presenting cells (APC's) and presented on the surface of their cell membranes in order for helper T (Th) cells to recognize the antigen and activate the immune response to act against it. |
|
|
Term
| What is the importance of Human Leukocyte Antigen (HLA)? |
|
Definition
| HLA provides the immune system with the ability to recognize foreign substance is foreign because the cellular fingerprint of the foreign substance will NOT match your unique cellular fingerprint. This will then set off the initial attack by APC's and subsequent activation of the rest of the immune system. |
|
|
Term
| What are the most common Type 1 Hypersensitivity disorders? |
|
Definition
| Hay fever, Asthma, Eczema, Food allergies, Anaphylaxis (Systemic) |
|
|
Term
| What is the primary type 1 characteristics? |
|
Definition
| it requires more than one exposure |
|
|
Term
| What are the key cells involved in Type 1 hypersensitivity? |
|
Definition
|
|
Term
| What are examples of allergens in Type 1 hypersensitivity? |
|
Definition
| Medications (penicillin, contrast dye), Biological agents (insect sting, vaccines), Foods (nuts, seafood, eggs), Yellow dye #5, Metals (Nickels, aluminum, zinc) |
|
|
Term
| What is the Primary (stage 1) stage of Type 1 Hypersensitivity? |
|
Definition
| First exposure, antibody production with Mast cell binding, cells are primed to go. |
|
|
Term
| What is the Secondary (stage 2) stage of Type 1 Hypersensitivity? |
|
Definition
| Subsequent exposure, rapid response, Sequence of events (Allergen binds to IgE, mast cell degranulation, mediator release) |
|
|
Term
| What is the genetic link of hyper-responsiveness and allergies? |
|
Definition
| High IgE levels, Reduced suppressor T cells. |
|
|
Term
| What are the manifestations of type 1 hypersensitivity? |
|
Definition
| Potent vasodilation (stuffy nose, lower BP), increased vascular permeability (edema, runny nose), bronchial smooth muscle contraction/constriction (breathing difficulties, wheezing), Leukocytes chemotaxis (none directly, attracts WBC's to area of inflammation/injury), pain associated w/ inflammation (discomfort). |
|
|
Term
| What are the manifestations of Systemic Anaphylaxis? |
|
Definition
| Smooth muscle contraction of bronchioles (can't breathe), Vasodilation of arterioles (BP drop), Increase in capillary permeability (swelling up) |
|
|
Term
| What is the primary characteristic of type 2 hypersensitivity? |
|
Definition
breaks down cells and blood cells. Destruction of targeted cells, antigens on cell stimulate antibody production. |
|
|
Term
| What are the primary antigens in Type 2 hypersensitivity? |
|
Definition
| IgG (primarily), WBC's, IgM |
|
|
Term
| What are example disorders of type 2? |
|
Definition
| Blood transfusion reaction (ABO incompatibility), Newborn ABO and RH, autoimmune disorders (Hemolytic Anemia, Myasthenia Gravis, Graves disease), Certain drug reactions |
|
|
Term
| What common signs and symptoms of Type 2? |
|
Definition
| Systemic (Chills, fever), Pulmonary (Dyspnea, coughing, cyanosis, wheezing, crackles, pulmonary edema), Integumentary (itching, rash, urticara/hives), Hematologic (abnormal bleeding), Neuro (H/A, uneasy feeling), Renal (Hemoglobinuria, oliguria/anuria), Other (chest/back pain, myalgia) |
|
|
Term
| What are the characteristics of Type 3 immune complex hypersensitivity? |
|
Definition
| Circulating AB (antibody) react with free AG (Antigen), formation of Ag-Ab complexes, deposit in tissues (kidneys, blood vessels, joints and skin) |
|
|
Term
| What is the underlying cause of tissue damage in type 3 hypersensitivity? |
|
Definition
| Triggering of the compliment cascade |
|
|
Term
| What can precipitate a type 3 response? |
|
Definition
| Persistent low grade infection (chronic immune complex production), Extrinsic environmental antigens (inhaled antigen), Autoimmune process (auto antibodies attack self-antigens |
|
|
Term
| What are the chain of events for type 4 hypersensitivity? |
|
Definition
| Sensitized T cells attack antigen and release lymphokines, lymphokines attract macrophages into contaminated area, macrophages cause damages |
|
|
Term
| What are the major characteristics for type 4? |
|
Definition
| T cell response to an allergen (antigen). No antibodies involved at all. |
|
|
Term
| What is the cause of delay in type 4? |
|
Definition
| T cell migration and accumulation |
|
|
Term
| What is the onset and progression for type 4? |
|
Definition
| begin to appear 24 hrs. after exposure. Reach max intensity 1-3 days. Damage can be extensive. |
|
|
Term
| What are example disorders for type 4? |
|
Definition
| Contact dermatitis (includes poison ivy), Organ transplants (chronic graft rejection), TB skin test |
|
|
Term
| What are the pharmacotherapy options for hypersensitivity reactions? |
|
Definition
| Immunosuppressants, antihistamines, epinephrine |
|
|
Term
| What do the pharmacotherapy options (Immunosuppressants, antihistamines, epinephrine) do? |
|
Definition
| Antihistamines (Suppress histamine mediator activity), Immunosuppresant's (Suppress cell-mediated immunity, anti-inflammatory), Epinephrine (halts mediator activity) |
|
|
Term
| What are the classifications, indication, attack, and major SE of epinephrine? |
|
Definition
Classification: Vasopressor, bronchodilator, anti-ashmatic, vasoconstriction. Indication: Severe allergic reactions, cardiac arrest, sever asthmatic attack Attack: inhibits release of mediators from mast cells SE: Cardiovascular (Angina, Arrhythmias, HTN, Tachycardia) Central Nervous System (Nervousness, Restlessness, Tremor) |
|
|
Term
| What is the route, dosage and how supplied for Epinephrine? |
|
Definition
Routes: All except PO, SQ is preferred Dosage: Adults (0.2 to 1 mg) Peds (.o1/mg/kg) Supplied: 1 mg in 1 ml vial (1:1000) |
|
|
Term
| What are the nursing implications for epinephrine? |
|
Definition
Monitor: V.S. and for status of reversal of symptoms. Correct dosage is crucial. for SQ use a TB syringe. For home use - teach how to correctly use adn contact clinican right after taking |
|
|
Term
| What is Anemia? and what does it result in? |
|
Definition
| Anemia is abnormally low number of circulating RBC's or Hgb level, which results in diminished oxygen carrying capacity. |
|
|
Term
| What does the severity of clinical manifestations of anemia depend on? |
|
Definition
| Severity of Anemia: (Asess RBC, Hgb & Hct - the lower they are the more severe the symptoms) Rate of Onset: (Fast/acute: body wont be able to compensate fast enough, person will experience a lot more symptoms. Slow: Body has good compensatory mechanisms, patient will have increased BP, HR, and Resp. to compensate for blood loss, the body will work harder an be pumping more blood to get it to circulate and pick up more oxygen for tissue.) Compensatory mechanisms: (Assess V.S. and RBC's, if body is compensating then V.S. should be increased.) Individual Factors:(Age extremes, general health status) |
|
|
Term
| What are types of Decreased RBC production anemias? |
|
Definition
| Iron deficiency anemia (most common), Aplastic Anemia, Chemotherapy induced |
|
|
Term
| What are types of increased RBC destruction Anemias? |
|
Definition
| Hemolytic Anemias (Sickle Cel Anemia, Hemolytic disease of newborn, Antibody mediated drug reactions) |
|
|
Term
| What are types of Increased RBC loss anemias? |
|
Definition
| Hemorrhage, Chronic bleeding, frequent blood sampling |
|
|
Term
| What are major causes of Iron deficiency Anemia (decreased RBC production)? |
|
Definition
| Chronic blood loss, deficient dietary intake (infancy), Increased demand (pregnancy & lactation). |
|
|
Term
| What are clinical manifestations of Iron deficiency Anemia? |
|
Definition
| Same as those of anemias, Epithelial atrophy (brittle hair and nails, smooth tounge, mouth sores, GI). Possible dysphagia and decreased acid secretions. |
|
|
Term
| What is the underlying patho of Primary hemolytic Anemia? |
|
Definition
| Mutated genes altering hemoglobin or erythrocyte structure and function |
|
|
Term
| what is acquired hemolytic anemia? |
|
Definition
| Premature destruction of RBC's caused by some external agent |
|
|
Term
| What are common causes of acquired hemolytic anemia? |
|
Definition
| Immune disorders (autoimmune attack, blood incompatibilities: ABO blood type, Rh factor. Certain drugs, Other: Physical agents, microangiopathies) |
|
|
Term
| In hemolytic Anemia what do you look for? |
|
Definition
| Reflection of RBC destruction, Increased reticulocyte count (Reticulocyte = immature RBC's), Mild jaundice, hemoglobinuria (red urine), hemoglobinemia (low circulating blood). |
|
|
Term
| What is a common cause of acute bleeding? and what labs do you look for? |
|
Definition
| Hemorrhage (trauma, GI bleeding). Labs: RBC, Hgb & Hct. Normal size and color. Rapid decrease r/t hemodilution. |
|
|
Term
| What is Aplastic Anemia? and what does it result in? |
|
Definition
| Primary condition of bone marrow stem cells. It results in...(figure out) |
|
|
Term
|
Definition
| an abnormally high total RBC mass |
|
|
Term
| what are the causes of primary polycythemia (polycythemia Vera)? |
|
Definition
| Cause: Excessive production of erythrocyte precursors in bone marrow. Myeloproliferative disease (effects all blood cells except Lymphocytes). How develops: Abnormality in pluripotential stem cells. |
|
|
Term
| What are the causes, purpose, and goal of secondary polycythemia? |
|
Definition
| Cause: Adaptive (compensatory) response to tissue hypoxia. Purpose: "Build more boats". Goal: Provide more oxygen carriers by increasing RBC production. |
|
|
Term
| Who develops secondary polycythemia? |
|
Definition
| Patients with chronic pulmonary and chronic heart problems |
|
|
Term
| With the four stage classification system. What is the Stage 1 of cancer? |
|
Definition
|
|
Term
| With the four stage classification system. What is the Stage 2 of cancer? |
|
Definition
|
|
Term
| With the four stage classification system. What is the Stage 3 of cancer? |
|
Definition
|
|
Term
| With the four stage classification system. What is the Stage 4 of cancer? |
|
Definition
|
|
Term
| In the TNM classification system, what does T=0 mean? |
|
Definition
| No evidence of primary tumor |
|
|
Term
| In the TNM classification system, what does T=IS mean? |
|
Definition
|
|
Term
| In the TNM classification system, what does T=1-4 mean? |
|
Definition
| Progressive increase in tumor size or involvement |
|
|
Term
| In the TNM classification system, what does N=0 mean? |
|
Definition
| No spread to regional lymph nodes |
|
|
Term
| In the TNM classification system, what does N=1 mean? |
|
Definition
| Spread to closest or small # of regional lymph nodes |
|
|
Term
| In the TNM classification system, what does N=2 mean? |
|
Definition
| Spread to most distant or numerous regional lymph node |
|
|
Term
| In the TNM classification system, what does M=0 mean? |
|
Definition
|
|
Term
| In the TNM classification system, what does M=1 mean? |
|
Definition
|
|
Term
| In the Stage theory of Carcogenesis. What is the initiation stage? |
|
Definition
| Initiation: Irreversible mutation = acting agent is a carcinogen, the "initiated cell" is not a cancer cell, it requires more mutation |
|
|
Term
| In the Stage theory of Carcogenesis. What is the promotion stage? |
|
Definition
| Promotion: Reversible proliferation of initiated cells = time it takes for initial cell mutation to develop into cancer, acting agent is promoters. |
|
|
Term
| In the Stage theory of Carcogenesis. What is the progression stage? |
|
Definition
| Progression: Clinical cancer, = invasion metastasis. |
|
|
Term
| In the cell cycle, what phase is G=0? |
|
Definition
|
|
Term
| In the cell cycle, what phase is G=1? |
|
Definition
|
|
Term
| In the cell cycle, what phase is S=1? |
|
Definition
|
|
Term
| In the cell cycle, what phase is G=2? |
|
Definition
|
|
Term
| In the cell cycle, what phase is M? |
|
Definition
|
|
Term
| In the cell cycle, what phase is M? |
|
Definition
|
|