Drugs For The Immune System

Front 1

WHAT CELLS ARE INVOLVED IN NONSPECIFIC IMMMUNITY?

Back 1

The phagocytes-->granulocytes & agranulocytes.

Front 2

WHAT CELLS ARE INVOLVED IN SPECIFIC IMMUNITY?

Back 2

The lymphocytes-->T cells & B cells.

Front 3

WHERE ARE LYMPHOCYTES MADE?

Back 3

The thymus and the bone marrow.
THYMUS=cell mediated-->T lymphocytes
BONE MARROW=humoral mediated-->B lymphocytes.

Front 4

WHAT ARE MHC AND WHAT ARE THE TWO DIFFERENT KINDS OF MHC?

Back 4

MHC are markers that determine which antigens an individual's B celss, T cells and macrophages can respond to. The different kinds of MHC are:
MHC I-markers that appear on all body cells and are the markers on all genes for SELF.
MHC II-markers that are found on B cells and macrophages responsible for presenting foreign antigens.

Hint 4

NOTE:
MHC I=SELF & MHC II=FOREIGN

Front 5

WHAT ARE THE FOUR WAYS THE BODY RECOGNIZES AN ANTIGEN?

Back 5

1.) Memory B cells can recognize a prototype of an antigen when it's present.
2.) T helper cells look for a class MHC II molecule (displayed by macrophage and B cells) on a NONSELF antigen.
3.) Cytotoxic T helper cells respond to MHC I class molecules found on all body cells.
4.) Some cytotoxic helper cells track down microbes while others become NKC(natureal killer cells).

Front 6

WHAT ARE CYTOKINES?

Back 6

-Cytokines are chemical communicator made of proteins.
-It posess multiple effects influencing production of other cytokines via cascade effects.
-Cytokines produced by lymphocytes are called LYMPHOKINES
-Cytokines produced by monocytes are called MONOKINES.

Front 7

WHAT ARE INTERFERONS?

Back 7

Interferons are cytokines secreted by cells invaded by viruses+others. It prevents viral replication and suppress malignant cell replication and tumor growth.

Front 8

WHAT ARE INTERLEUKINS?

Back 8

Interleukins are cytokines secreted by active WBCs that influence other WBCs.

Front 9

WHAT ARE THE TWO TYPES OF INTERLEUKINS?

Back 9

The two types of interleukins are:
IL-1=stimulates T cells to initiate immune response.
IL-2=released from active T cells to stimulate the production of more T cells and increase activity of B cells, cytotoxic cells and natural killer cells.

Hint 9

NOTE:
IL-1=stimulates T cells
IL-2=released from T cells to stimulate more T cells.

Front 10

WHAT CELLS ARE INVOLVED IN NONSPECIFIC IMMMUNITY?

Back 10

The phagocytes-->granulocytes & agranulocytes.

Front 11

WHAT CELLS ARE INVOLVED IN SPECIFIC IMMUNITY?

Back 11

The lymphocytes-->T cells & B cells.

Front 12

WHERE ARE LYMPHOCYTES MADE?

Back 12

The thymus and the bone marrow.
THYMUS=cell mediated-->T lymphocytes
BONE MARROW=humoral mediated-->B lymphocytes.

Front 13

HOW DO T CELLS DEVELOP?

Back 13

-T-cells first leave the thymus and are referred to as "naive" until their initial encounter with an antigen.
-Following antigenic stimulation, a single cell expands into a pool of cells, with some forming memory which will regain activity with repeated stimulation/exposure.

Front 14

WHAT CELLS ARE INCLUDED IN THE T-CELL GROUP?

Back 14

T-cells include the:
-cytotoxic T lymphocytes
-functional subsets of T cells characterized by their cytokine secretion profiles.

Front 15

WHAT ARE CYTOTOXIC T CELLS AND HOW DO THEY FUNCTION?

Back 15

Cytotoxic T cells are a type of lymphokine and has several modes of action:
-cytotoxic T cells respond to specific antigens/antibody complexes on plasma cells and kill on contact.
-cytotoxic T cells secrete messengers called lymphokines
-a subset of cytotoxic T cells are called Natural Killer Cells (NKC).
-cytotoxic cells also become suppressor T cells.

Front 16

WHAT ARE NATURAL KILLER CELLS AND HOW DO THEY FUNCTION?

Back 16

-Natural Killer Cells are a type of cytotoxic T cell.
-Unlike the regular cytotoxic T cell, NKC do not need to recognize a specific antigen.
-NKC recognize class MHC 1(self) proteins, so it targets tumor cells and protects against a variety of microbes.
-NKC spontaneously destroys malignant cells.
-NKS patrols the body & kills on contact by delivering bursts of letal lymphokines.

Hint 16

NOTE: Know that NKC patrols the body & kills on contact by delivering a burst of lethal lymphokines.

Front 17

WHAT ARE B-CELLS AND HOW DO THEY DEVELOP IN THE BODY?

Back 17

-B-cells are programmed to identify specific antigens.
-When B-cells reacts with it's specific antigen, it changes into a plasma cells which produce immunoglobulins.
-An antigen-antibody complex is formed and activates a series of plasma proteins called complement.
-The complement proteins then destroy antigens.

Front 18

WHAT ARE THE FIVE DIFFERENT COMPLEMENT IMMUNOGLOBULINS AND WHAT ARE THE FUNCTIONS OF EACH?

Back 18

1.) IgG=kills bacteria
2.) IgA=viral protection in secretions, GI
3.) IgM=kills bacteria
4.) IgE=for allergy & wards off parasites*
5.) IgD=regulates cell activation

Hint 18

NOTE: IgGAMED

Front 19

DURING ALLERGIC REACTION, WHICH CELLS SIGNALS THE ALLERGIC REACTION?

Back 19

The eosinophils and basophils signal the allergic reaction. The allergic reaction is regulated by the immunoglobuline IgE.

Front 20

DURING BACTERIAL INFECTION, WHICH MUST THE NURSE BE ALERT TO IN THE PATIENT'S LAB RESULTS?

Back 20

During a bacterial infection, the nurse must be alert to the neutrophil levels because the mature cells could run out and result in a SHIFT TO THE LEFT(increased BANDS), meaning that the immature cells from the bone marrow are being used up.

Front 21

WHICH CELL PRODUCES THE IMMUNOGLOBULIN COMPLEXES?

Back 21

The B-cells are differentiated into the different immunoglobulin complexes.

Front 22

DESCRIBE THE IgE Type 1 Hypersensitivity PROCESS/PATHWAY.

Back 22

1.) The first time the allergy-prone person runs across an allergen such as ragweed, he or she makes large amounts of ragweed IgE antibody.
2.) The IgE molecules will then attach themselves to mast cells.
3.) The second time that person has a brush with ragweed, the IgE primed mast cells will release its powerful chemicals and the person will suffer the wheezing and/or sneezing, runny nose, watery eyes, and itching of allergy.

Front 23

WHAT ARE THE THREE RELATIONSHIPS BETWEEN IMMUNE SYSTEM AND CANCER?

Back 23

1.) Immune system can sometimes cause a spontaneous remissions in ptients with cancer.
2.) There is an increased incidence of cancer in immunosuppressed patients.
3.) It has been shown that there is presence of lymphoid infiltrates in solid tumors.

Front 24

WHAT ARE SOME OF THE KNOWN AUTOIMMUNE DISEASES?

Back 24

-Rheumatoid arthritis
-Systemic lupus erythematosus
-Type I diabetes mellitus
-Myasthenia gravis
-Graves' disease
-Multiple sclerosis
-Sjogren's syndrome

Front 25

WHAT ARE THE DIFFERENT ETIOLOGIES OF AUTOIMMUNE DISORDERS?

Back 25

-Genetics
-Viruses
-Environmental factors
-Drugs
-Sex hormones (more common in women)
-Multiple unknown causes

Front 26

WHICH CELL PRODUCES THE IMMUNOGLOBULIN COMPLEXES?

Back 26

The B-cells are differentiated into the different immunoglobulin complexes.

Front 27

DESCRIBE THE IgE Type 1 Hypersensitivity PROCESS/PATHWAY.

Back 27

1.) The first time the allergy-prone person runs across an allergen such as ragweed, he or she makes large amounts of ragweed IgE antibody.
2.) The IgE molecules will then attach themselves to mast cells.
3.) The second time that person has a brush with ragweed, the IgE primed mast cells will release its powerful chemicals and the person will suffer the wheezing and/or sneezing, runny nose, watery eyes, and itching of allergy.

Front 28

WHAT ARE THE THREE RELATIONSHIPS BETWEEN IMMUNE SYSTEM AND CANCER?

Back 28

1.) Immune system can sometimes cause a spontaneous remissions in ptients with cancer.
2.) There is an increased incidence of cancer in immunosuppressed patients.
3.) It has been shown that there is presence of lymphoid infiltrates in solid tumors.

Front 29

WHAT ARE SOME OF THE CAUSES OR PATHOPHYSIOLOGIES IN AUTOIMMUNE DISEASES?

Back 29

In general, autoantibodies are present in the many autoimmune diseases. Some of the pathophysiologies in autoimmune diseases are:
1.) Antibodies are directed against substances found in the cell's DNA, RNA and link up with SELF antigens.
2.) The MHC I(self) markers for self are no longer recognized as SELF and are seen as forein antigen.
3.) The immune complex set off inflammatory reactions.
4.) B-cells might be hyperactive while cytotoxic T suppressor cells may be underactive.
5.) T cell receptor may be defective or ineffective being capable of damagin own tissues.

Front 30

WHAT ARE SOME OF THE NON-PHARMACOLOGIC TREATMENTS FOR AUTOIMMUNE DISEASE?

Back 30

-Stress reduction
-Exercise to increase energy (low impact)
-Rest fo restorative functions
-Physical Therapy
-Massage therapy
-Vitamin/mineral supplements such as Vitamin C, Vitamin E and Glucosamine/Chondroitin

Front 31

WHAT ARE SOME OF THE PHARMACOLOGIC TREATMENTS FOR AUTOIMMUNE DISEASES?

Back 31

-NSAIDs + COX-2 inhibitors
-Corticosteroids
-Immunosuppresant agents
-Disease-modifying anti-rheumatic drugs (DMARDs)
-New biologic therapies

Front 32

HOW DO GLUCOCORTICOIDS WORK?

Back 32

-Glucocorticoids work by suppressing lymphocyte, inflammation and immune reactions.
-It is well-absored from the GI
-Hydrocortisone and prednisolone do not require hepatic metabolism to active form, which is why it's the short & intermediate-acting glucocorticoid drugs.

Front 33

WHAT ARE THE THREE DIFFERENT CLASSES OF GLUCOCORTICOIDS?

Back 33

1.) Short-acting=HYDROCORTISONE
2.) Intermediate-acting=PREDNISOLONE
3.) Long-acting=DEXAMETHASONE

Front 34

WHAT ARE THE SHORT TERM ADVERSE EFFECTS OF GLUCOCORTICOIDS?

Back 34

-Sodium retention=WEIGHT GAIN
-Hyperglycemia
-Adrenal suppression
-Mood changes
-Insomnia
-Stomach upset

Hint 34

NOTE: SHAMIS

Front 35

DUE TO GLUCOCORTICOID'S EFFECT OF ADRENAL SUPPRESION, WHAT PRECAUTION MUST BE TAKEN?

Back 35

The patient must be tapered off slowly from glucocorticoid therapy due to its effect of adrenal suppression which could result in secondary adrenocortical insufficiency. What happens is, if the glucocorticoid medication is abruptly withdrawn, the shrunken adrenal glands from prolonged glucocorticoid therapy will not be able to secrete sufficient glucocorticoids & symptoms of acute adrenocortical insufficiency will appear.

Front 36

WHAT ARE THE LONG-TERM SIDE EFFECTS OF GLUCOCORTICOIDS?

Back 36

-Muscle atrophies
-Thin skin
-Bone loss
-Peptic ulcers
-Weight redistributed (buffalo hump)
-Cataracts & glaucoma
(NOTE: Cushingoid signs & symptoms)

Front 37

WHAT ARE THE DIFFERENT TYPES OF BIOLOGICAL THERAPY?

Back 37

1.) Hematopoeitic growth factors (ANEMIA)
2.) Colony stimulating factors
3.) Cytokines
4.) Polyclonal/monoclonal antibodies
5.) Immune modulators

Front 38

WHAT ARE THE VARIOUS WAYS BIOLOGICAL AGENTS WORK?

Back 38

-Stimulates host defense cells by functioning as singaling systems mainly via cytokine responses.
-Stimulates growth of new cells from bone marrow.
-Disrupts host/tumor relationship by acting on tumor vasculature and nutrient supply.
-Used as immune suppresants
-Used concurrently to treat certain autoimmune disorders and cancers.
-It has potentially many exciting possibilities

Front 39

HOW DO BIOLOGIC THERAPY UNDER COLONY-STIMULATING FACTOS WORK?

Back 39

Colony-stimulating factors work by:
-increasing the numbers of various immune cells
-binding to receptors on specific progenitor cells in bone marrow
-produced by recombinant DNA technology which allows human protein to be engineered

Front 40

WHAT ARE SOME OF THE CURRENT COLONY STIMULATING AGENTS AND HOW DO THEY WORK?

Back 40

Some of the current colony-stimulating agents are produced recombinant granulocyte-macrophage that cause bone marrow to increase production of neutrophils.
1.) Pegfilgastrim (Neulasta) & Filgastrim (Neupogen)=works by returning cell-mediated immunity to the patient; used to shorten febrile neutropenia induced b myelosuppressive antineoplastic drugs; recombinantly engineered from E.coli bacteria.
2.) Neurogen=approved for adult myelogenous leukemia and for pats after bone marrow transplant.
3.) Sargramostim (Leukine)=works by producing more than one type of cell (neutrophil & monocytes); is recombinantly engineered granulocyte-macrophage from yeast cells; used after bone marrow transplant & in adults with acute myelogenous leukemia & non-Hodgkin's lymphoma.

Front 41

WHAT ARE THE COMMON SIDE EFFECTS OF COLONY-STIMULATING FACTORS?

Back 41

-Bone pain
-Risk for further leukemic progression
-Fever
-Allergic reactions, esp to pts sensitive to proteins derived from E.coli bacteria. (pt. can have respiratory distress.)

Front 42

WHAT SIDE EFFECT CAN SOME PATIENTS HAVE TO SARGRAMOSTIM?

Back 42

Sargramostim can cause capillary leak syndrome with peripheral edema and pleural effusion with SOB and hypotension.

Front 43

WHAT IS CYTOKINE THERAPY AND HOW DOES IT WORK?

Back 43

Cytokines are proteins released by WBCs in response to antigenic invasion.
-Cytokine therapy enhances and accelerates the inflammatory and specific responses that will destroy invading antigen.
-Cytokine therapy has proinflammatory with anti-viral, anti-proliferative, and anti-neoplastic properties.

Front 44

WHAT ARE SOME OF THE CURRENT CYTOKINE AGENTS USED?

Back 44

Cytokine agents for Cytokine Therapy are generally Interferons and Interleukins produced by activated lymphocytes.

Front 45

WHAT ARE THE COMMON SIDE EFFECTS OF CYTOKINE THERAPY?

Back 45

-Dizziness, confusion, lethargy
-Flu-like symptoms
-Anorexia, nausea
-Depression and suicidal ideation
-Bone marrow depression
-Increased liver enzymes
**NOTE: The above can result in -risk for infection, -risk for injury, -altered nutrition less than body requirements.

Front 46

WHAT IS POLYCLONAL/MONOCLONAL ANTIBODIES AND WHAT ARE THEY USED FOR?

Back 46

Note: Only monoclonal antibodies used now. Monoclonal antibodies are used to react with specific tumor receptor sites for diagnosis and treatment of malignancy.

Front 47

NAME SOME OF THE COMMON MONOCLONAL ANTIBODY AGENTS (Specific to what's already been mentioned in class)?

Back 47

1.) For treatment of RA:
-infliximab (Remicade)=for tx of RA, binds to TNF & unlike other monoclonal antibodies, it has no anti-tumor function.
-adalimumab (Humira)
2.) For antiplatelet:
-Abciximab (Reopro)-binds to GPIIb/IIIa on human platelets to help prevent platelet aggregation.
3.) For treatment of breast cancer:
-trashuzumab (Herceptin)=recombinant DNA-derived humanized monoclonal antibody for tx of breast cancer in those who has over expression of HER2 protein.

Front 48

WHAT ARE IMMUNE MODULATORS AND HOW DO THEY WORK?

Back 48

-Immune modulators act directly on function of T & B cells and can either stimulate or suppress the immune response
-Those that act as suppressants block the normal effects of the immune system; therefore, it is BENEFICIAL FOR ORGAN TRANSPLANTATION AND IN AUTOIMMUNE DISEASE.

Front 49

HOW DOES TNF (TUMOR NECROSIS FACTOR) PLAY A ROLE IN RA PATHOGENESIS?

Back 49

TNF is a cytokine that stimulates other cytokines-interleukins(IL) and causes massive inflammatory response. TNF also inhibits some bone formation, induces resorption and stimulates secretion of protein-degrading enzymes to destroy joints.

Front 50

WHAT ARE THE PHARMACOLOGIC TREATMENTS FOR RA?

Back 50

-NSAIDS & COX-2 inhibitors
-Corticosteroids=Prednisone & NI: monitor wt, glucose & osteoporosis
-DMARDs=slows the progression of the disease.
Example:
1.) Methotrexate(Rheumatrex)=most widely used because of LONG-TERM EFFICACY; may add other DMARDs to regimen to increase efficacy and reverse debilitating effects of RA. S/E: oral ulcers, nausea, anorexia, increase risk for infection--must monitor CBC
**NOTE: Methotrexate is an anti-cancer drug that lowers immune function.
2.) Leflunomide(Arava)=used w/ Methotrexate; its a cytostatic agent & an immunosuppressant that inhibits synthesis of pyrimidine required for proliferation of Tcells; also inhibits IL1 and TNF alpha. S/E: skin rash, abd pain, diarrhea, nausea, reversible alopecia--must monitor for increased LFTs.

Front 51

WHAT PRECAUTION SHOULD BE TAKEN FOR A PATIENT WHO IS ON PHARMACOLOGIC TREATMENT SPECIFICALLY "BIOLOGIC THERAPY" FOR RA?

Back 51

Nurse must note that all RA Biologic Therapy drugs are not recommended for patients with latent TB and has history of cancer malignancy because it can cause increased risk for infection.

Front 52

WHAT IS THE MODE OF ACTION OF etanercept (Enbrel)?

Back 52

Etanercept (Enbrel) is a TNF-alfpha blocker. During RA increased inflammation, immune system counteracts with its own anti-inflammatory agents. One is a receptor for TNF which this drug binds to and inactivates the excess TNF-alpha.

Front 53

WHICH TNF BLOCKER FOR TREATMENT OF RA IS NOT USED WITH OTHER TNF BLOCKERS?

Back 53

Adalimumab (Humira) is given by SQ and not concurrently with other TNF blockers.

Front 54

WHICH DRUG FOR TREATMENT OF RA UNDER THE BIOLOGIC THERAPY IS NOT A TNF BLOCKER?

Back 54

Anakinra (Kineret) because it is an interleukin 1 (IL1) receptor antagonist. The MOA is to augment the diminished levels of naturally occuring IL1 as a counterbalance to the detrimental effects of IL1 activity in bone resorption, erosion and and joint cartilage destruction.