lOMoAR cPSD| 67691079
Week 1 Immune Response
Hypersensitivity Reactions
Type I Allergic Reactions
● Examples of hypersensitivity reactions—include hay fever, anaphylaxis, and food allergies.
● Mechanism—Immune globulin E (IgE), produced by B-lymphocytes, binds to the mast cells and releases
histamine and chemical mediators.
● Localized Effect—Inflammation (edema, redness, and pruritis); additional symptoms may be present, depending
on the tissues and organs involved.
● Systemic Effect (Anaphylaxis)—The most severe Type 1 reaction results from large amounts of chemical
mediators being released into general circulation quickly. Symptoms include decreased blood pressure, airway
obstruction, pruritis, and severe hypoxia.
Type II Cytotoxic Hypersensitivity
● Examples of cytotoxic hypersensitivity reactions—Include incompatible blood transfusion and Rh factor
incompatibility, blood transfusion, HIT, Grave’s disease (hyperthyroidism)
● Mechanism—IgG or IgM reacts with the antigen on the cell and the complement is activated.
● Effect—The transfusion with incompatible ABO-type blood causes red blood cell lysis and phagocytosis. The
recipient’s symptoms result from the loss of cell function and intravascular immune reactions including fever, chills,
pain (back and chest), low blood pressure, dark urine, and uncontrolled bleeding.
Type III Immune Complex Hypersensitivity
● Examples of immune complex hypersensitivity reactions—autoimmune disorders, lupus, glomerulonephritis,
Arthus reaction, rheumatoid arthritis, serum sickness, Reynaud phenomenon
● Mechanism—Antigen-antibody complex deposits in the tissue and complement is activated. ● Effect—
inflammation, tissue necrosis, and vasculitis
Type IV Cell-Mediated or Delayed Hypersensitivity
● Examples of cell-mediated (delayed) hypersensitivity reaction—organ transplant rejection, contact dermatitis,
positive tuberculin skin test, DM1, latex (can be type 1 as well, do not have avocado, banana, chestnut, kiwi,
passion fruit)
● Mechanism—Antigen binds to T lymphocyte and the sensitized lymphocyte releases lymphokines.
● Effect—delayed inflammation, tissue destruction
, lOMoAR cPSD| 67691079
* Difference between type 2 and 3: Type 2 is antigen-antibody bound at the cell surface, whereas type 3 is in circulation
and non-organ specific.
2
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, lOMoAR cPSD| 67691079
Immunodeficiency
First Line of Defense
Physical Barriers Mechanical Barriers Biochemical Barriers
● Skin ● Cilia ● Mucous
● Mucous membranes ● Coughing, Sneezing ● Perspiration
● Intestinal epithelium ● Urinating ● Saliva
● Vomiting ● Tears
● Defecation ● Earwax
Second Line of Defense
If foreign substances penetrate the first-line barriers, the non-specific inflammatory response rapidly senses non-self
invaders and sends immune resources to contain and neutralize the invading substance. Immune resources include the
following:
● neutrophils
○ first responders that marginate, diapedeses, and phagocytize
● monocytes and macrophages
○ phagocytize and release cytokines
● plasma protein systems activated
○ complement system
○ clotting system
○ kinin system
● platelet-activating factor ○ releasing more mediators to assist in increasing vascular permeability, helping immune
resources travel to the invader
● mast cells
○ releasing more inflammatory mediators
Third Line of Defense
Foreign antigens are phagocytized by antigen-presenting cells (macrophages and dendritic cells) and signal and bind to
CD4+ helper T-cells to activate them.
CD4+ helper T-cells control and coordinate host defense response through this mechanism. Then, CD4+ helper T-cells
activate CD8 cytotoxic T-cells, macrophages, B-cells, and NK cells through cytokine release.
, lOMoAR cPSD| 67691079
Cancer-induced immunodeficiency Risk Factors ●
Intrinsic Risk Factors
○ The ability of cancer cells to modify their antigenic expression and secrete substances that dampen immune
responses directly contributes to immune suppression.
○ Production of cytokines and chemokines by tumor cells can hinder the proliferation and activation of immune
cells, suppressing the immune response.
● Extrinsic Risk Factors:
○ Factors contributing to the poor underlying health of the client, including malnutrition, age-related immune
decline, and comorbidities such as diabetes or HIV can weaken the immune response.
○ Lifestyle and environmental factors, such as smoking or chemical exposure, can further weaken the immune
response.
● Treatment-Related Risk Factors
○ Therapeutic interventions like chemotherapy, radiation, and other immunosuppressive drugs can cause bone
marrow suppression, leading to neutropenia. Neutropenia significantly increases infection risk.
○ Clients with cancer requiring surgery and in the post-operative recovery phases may experience reduced
immune surveillance, leading to increased susceptibility to opportunistic infections.
Cancer-induced immunodeficiency
● Infection: more frequent and severe infections from opportunistic infections. Neutropenia can predispose pt to
infection, LIFE-THREATENING, especially in fever
4
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Week 1 Immune Response
Hypersensitivity Reactions
Type I Allergic Reactions
● Examples of hypersensitivity reactions—include hay fever, anaphylaxis, and food allergies.
● Mechanism—Immune globulin E (IgE), produced by B-lymphocytes, binds to the mast cells and releases
histamine and chemical mediators.
● Localized Effect—Inflammation (edema, redness, and pruritis); additional symptoms may be present, depending
on the tissues and organs involved.
● Systemic Effect (Anaphylaxis)—The most severe Type 1 reaction results from large amounts of chemical
mediators being released into general circulation quickly. Symptoms include decreased blood pressure, airway
obstruction, pruritis, and severe hypoxia.
Type II Cytotoxic Hypersensitivity
● Examples of cytotoxic hypersensitivity reactions—Include incompatible blood transfusion and Rh factor
incompatibility, blood transfusion, HIT, Grave’s disease (hyperthyroidism)
● Mechanism—IgG or IgM reacts with the antigen on the cell and the complement is activated.
● Effect—The transfusion with incompatible ABO-type blood causes red blood cell lysis and phagocytosis. The
recipient’s symptoms result from the loss of cell function and intravascular immune reactions including fever, chills,
pain (back and chest), low blood pressure, dark urine, and uncontrolled bleeding.
Type III Immune Complex Hypersensitivity
● Examples of immune complex hypersensitivity reactions—autoimmune disorders, lupus, glomerulonephritis,
Arthus reaction, rheumatoid arthritis, serum sickness, Reynaud phenomenon
● Mechanism—Antigen-antibody complex deposits in the tissue and complement is activated. ● Effect—
inflammation, tissue necrosis, and vasculitis
Type IV Cell-Mediated or Delayed Hypersensitivity
● Examples of cell-mediated (delayed) hypersensitivity reaction—organ transplant rejection, contact dermatitis,
positive tuberculin skin test, DM1, latex (can be type 1 as well, do not have avocado, banana, chestnut, kiwi,
passion fruit)
● Mechanism—Antigen binds to T lymphocyte and the sensitized lymphocyte releases lymphokines.
● Effect—delayed inflammation, tissue destruction
, lOMoAR cPSD| 67691079
* Difference between type 2 and 3: Type 2 is antigen-antibody bound at the cell surface, whereas type 3 is in circulation
and non-organ specific.
2
messages.downloaded_by performance
, lOMoAR cPSD| 67691079
Immunodeficiency
First Line of Defense
Physical Barriers Mechanical Barriers Biochemical Barriers
● Skin ● Cilia ● Mucous
● Mucous membranes ● Coughing, Sneezing ● Perspiration
● Intestinal epithelium ● Urinating ● Saliva
● Vomiting ● Tears
● Defecation ● Earwax
Second Line of Defense
If foreign substances penetrate the first-line barriers, the non-specific inflammatory response rapidly senses non-self
invaders and sends immune resources to contain and neutralize the invading substance. Immune resources include the
following:
● neutrophils
○ first responders that marginate, diapedeses, and phagocytize
● monocytes and macrophages
○ phagocytize and release cytokines
● plasma protein systems activated
○ complement system
○ clotting system
○ kinin system
● platelet-activating factor ○ releasing more mediators to assist in increasing vascular permeability, helping immune
resources travel to the invader
● mast cells
○ releasing more inflammatory mediators
Third Line of Defense
Foreign antigens are phagocytized by antigen-presenting cells (macrophages and dendritic cells) and signal and bind to
CD4+ helper T-cells to activate them.
CD4+ helper T-cells control and coordinate host defense response through this mechanism. Then, CD4+ helper T-cells
activate CD8 cytotoxic T-cells, macrophages, B-cells, and NK cells through cytokine release.
, lOMoAR cPSD| 67691079
Cancer-induced immunodeficiency Risk Factors ●
Intrinsic Risk Factors
○ The ability of cancer cells to modify their antigenic expression and secrete substances that dampen immune
responses directly contributes to immune suppression.
○ Production of cytokines and chemokines by tumor cells can hinder the proliferation and activation of immune
cells, suppressing the immune response.
● Extrinsic Risk Factors:
○ Factors contributing to the poor underlying health of the client, including malnutrition, age-related immune
decline, and comorbidities such as diabetes or HIV can weaken the immune response.
○ Lifestyle and environmental factors, such as smoking or chemical exposure, can further weaken the immune
response.
● Treatment-Related Risk Factors
○ Therapeutic interventions like chemotherapy, radiation, and other immunosuppressive drugs can cause bone
marrow suppression, leading to neutropenia. Neutropenia significantly increases infection risk.
○ Clients with cancer requiring surgery and in the post-operative recovery phases may experience reduced
immune surveillance, leading to increased susceptibility to opportunistic infections.
Cancer-induced immunodeficiency
● Infection: more frequent and severe infections from opportunistic infections. Neutropenia can predispose pt to
infection, LIFE-THREATENING, especially in fever
4
messages.downloaded_by performance
