Immunity & Inflammation

Question 1

Inappropriate immune responses may be

Answer 1

(1) exaggerated against environmental antigens (allergy); (2) misdirected against the host’s own cells (autoimmunity); (3) directed against beneficial foreign tissues, such as transfusions or transplants (alloimmunity); or (4) be insufficient to protect the host (immune deficiency).

Question 2

Hypersensitivity

Answer 2

is an altered immunologic response to an antigen that results in disease or damage to the host.

Question 3

Hypersensitivity reactions can be classified in two ways:

Answer 3

by the source of the antigen that the immune system is attacking (allergy, autoimmunity, alloimmunity; and by the mechanism that causes disease (types I, II, III, and IV;

Question 4

Allergy

Answer 4

deleterious effects of hypersensitivity to environmental antigens, and immunity means the protective responses to antigens expressed by disease-causing agents.

Question 5

Autoimmunity

Answer 5

disturbance in the immunologic tolerance of self-antigens. The immune system normally does not strongly recognize the individual’s own antigens.

Question 6

autoimmune diseases

Answer 6

occur when the immune system reacts against self-antigens to such a degree that the person’s own tissues are damaged by autoantibodies or autoreactive T cells

Question 7

Alloimmunity (also termed isoimmunity)

Answer 7

occurs when the immune system of one individual produces a reaction against tissues of another individual. Alloimmunity can be observed during immunologic reactions against transfusions, transplanted tissue, or the fetus during pregnancy.

Question 8

Most diseases caused by hypersensitivity develop because

Answer 8

interactions of at least three variables: (1) an original “insult,” which alters immunologic homeostasis (a steady state of tolerance to self-antigens or lack of immune reaction against environmental antigens); (2) the individual’s genetic makeup, which determines the degree of the resultant immune response from the effects of the insult; and (3) an immunologic process that causes the symptoms of the disease.

Question 9

4 Mechanisms of Hypersensitivity

Answer 9

type I (immunoglobulin E [IgE]–mediated) hypersensitivity reactions, type II (tissue-specific) hypersensitivity reactions, type III (immune complex–mediated) hypersensitivity reactions, and type IV (cell-mediated) hypersensitivity reactions.

Question 10

anaphylaxis.

Answer 10

most rapid and severe immediate hypersensitivity reaction.
Occurs within minutes of reexposure to the antigen and can be either systemic (generalized) or cutaneous (localized).
S/S itching, erythema, headaches, n/v, abdominal cramps, diarrhea, difficult breathing. Sever: contraction of bronchial smooth muscle, laryngeal edema & vascular collapse=shock & death.

Question 11

Type I (IgE-mediated) hypersensitivity reactions

Answer 11

mediated by antigen-specific IgE and the products of tissue MAST CELLS (initiate and mediate)
Most common allergies (e.g., pollen allergies.The initial phase is characterized by vasodilation, vascular leakage, and, depending on the location, smooth muscle spasm or glandular secretions. These changes usually become evident within 5 to 30 minutes
EX: allergy to peanuts, anaphylaxis

Question 12

cytotropic antibody
(part of type 1).

Answer 12

Antibody that binds to mast cells(able to bind to cell surfaces) or reagin (skin-sensitizing antibody)

Question 13

The most potent mediator is
(Type 1 sensitivity)

Answer 13

Histamine. Acting through the H1 receptors, histamine contracts bronchial smooth muscles, causing bronchial constriction; increases vascular permeability, causing edema; and causes vasodilation increasing blood flow into the affected area.histamine with H2 receptors results in increased gastric acid secretion and a decrease of histamine released from mast cells and basophils.negative feed back mechanism that stops degranulation.
-important activity of histamine is enhancement of the chemotactic activity of other factors, such as eosinophil chemotactic factor of anaphylaxis (ECF-A), which attracts eosinophils into sites of allergic inflammatory reactions and prevents them from migrating out of the inflammatory site.

Question 14

Mast cells
(Type 1 sensitivity)

Answer 14

initiate synthesis of bioactive lipid-derived mediators, such as leukotrienes, platelet-activating factor (PAF), and prostaglandins.
Released much more slowly than histamine.
Can mediate similar, yet more prolonged, clinical symptoms, such as recruiting inflammatory cells (e.g., neutrophils, eosinophils), promoting vascular permeability and edema, inducing bronchoconstriction or rhinitis, and inducing further release of histamine from mast cells

Question 15

Type II (tissue-specific) hypersensitivity reactions

Answer 15

characterized by a specific cell or tissue being the target of an immune response.
Symptoms of many type II diseases are determined by which tissue or organ expresses the particular antigen.
1-cell can be destroyed by antibody (IgG or IgM) and activation of the complement cascade through the classical pathway, damages the membrane and may result in lysis.
2-antibody may cause cell destruction through phagocytosis by macrophages.
3-antibody and complement may attract neutrophils that trigger phagocytosis
4-antibody-dependent cell-mediated cytotoxicity (ADCC)- NK cells release toxic substances that destroy the target cell.
5-does not destroy the target cell, but rather causes it to malfunction.
EX: RH incompatible mother/baby, transfusion reaction.

Question 16

type III (immune complex–mediated) hypersensitivity reactions

Answer 16

caused by antigen-antibody (immune) complexes that are formed in the circulation and deposited later in vessel walls or extravascular tissues, type III the antibody binds to soluble antigen that was released into the blood or body fluids, and the complex is then deposited in the tissues. (causing autoimmune diseases)
Not organ specific, harmful effects caused by complement activation. Nuetrophils attempt to ingest the immune complexes
EX: SLE, serum sichness,Raynauds, rheumatoid arthritis.

Question 17

serum sickness
(Type 3)

Answer 17

systemic prototype of immune complex–mediated disease because it was initially described as being caused by the therapeutic administration of foreign serum, ex: after taking amoxicillin
S/S: fever, rash, joint pain
EX: Raynaud phenomenon, condition caused by the temperature-dependent deposition of immune complexes in the capillary beds of the peripheral circulation.

Question 18

type IV (cell-mediated) hypersensitivity reactions

Answer 18

mediated by T lymphocytes and do not involve antibody, Tc cells attack and destroy cellular targets directly.
Th1 and Th17 cells produce
cytokines that recruit and activate phagocytic cells, especially macrophages. Destruction of the tissue is usually caused by direct killing by toxins from Tc cells or by the release of soluble factors, such as lysosomal enzymes and toxic reactive oxygen species (ROS), from activated macrophages.
EX: Contact dermatitis from latex, graft rejection, rheumatoid arthritis(joint tissue), Hashimoto(thyroid), DM type 1(pancreatic beta cells)

Question 18

Arthus reaction
(Type 3)

Answer 18

prototypic example of a localized immune complex–mediated inflammatory response.6 It is caused by repeated local exposure to an antigen that reacts with preformed antibody and forms immune complexes in the walls of the local blood vessels

Question 19

clinical manifestations of type I reactions

Answer 19

biologic effects of histamine: tissues with large amounts of mast cells (GI, skin, respiratory)
Type 1 very common
primary mechanism of control is the autonomic nervous system. (target cells of inflammation)
Use of antihistamines

Question 20

type IV allergic reaction

Answer 20

haptens that react with normal self-proteins in the skin. contact dermatitis that is confined to the area of contact with the allergen

Question 21

Type II allergic hypersensitivities

Answer 21

usually against allergic haptens that bind to the surface of cells and elicit an IgG or IgM response.

Question 22

Type III allergic reactions

Answer 22

occur after the formation of immune complexes containing soluble allergens

Question 23

Tolerance

Answer 23

Tolerance is a state of immunologic control so that the individuals do not make a detrimental immune response against their own cells and tissues

Question 24

Central tolerance

Answer 24

develops in humans during the embryonic period as autoreactive lymphocytes are either eliminated or suppressed in the primary lymphoid organs during differentiation and proliferation of immature T or B lymphocytes. Clones of cells with antigen receptors for self-antigens are deleted

Question 25

Peripheral tolerance

Answer 25

is maintained in the secondary lymphoid organs through the action of T-regulatory lymphocytes or antigen-presenting dendritic cells. **Autoimmune disease results more commonly from a breakdown of this peripheral tolerance rather than a defect in central tolerance.

Question 26

neoantigens

Answer 26

(new antigens) are haptens that become immunogenic after binding to self-proteins

Question 27

alloimmunity

Answer 27

when an individual's immune system reacts against antigens on the tissues of other members of the same species. EX: blood transfusion or organ transplant

Question 28

Systemic lupus erythematosus (SLE)

Answer 28

chronic, multisystem, inflammatory disease and is one of the most common, complex, and serious of the autoimmune disorders. characterized by multiple immune disorders that result in the B- and T-cells become overactive, increasing autoantibodies against nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and many other self- components (complement system). antibody against DNA produces tissue damage in individuals. causes inflammatory lesions in the renal tubular basement membranes, brain (choroid plexus), heart, spleen, lung, gastrointestinal tract, skin and peritoneum. Scar formation women, 20-40, black. prolonged us of hydralazine & procainamide.

Question 29

SLE S/S

Answer 29

1. Facial rash confined to the cheeks (malar rash) 2. Discoid rash (raised patches, scaling) 3. Photosensitivity (development of skin rash developed as a result of exposure to sunlight) 4. Oral or nasopharyngeal ulcers 5. Nonerosive arthritis of at least two peripheral joints 6. Serositis (pleurisy, pericarditis) 7. Renal disorder (persistent proteinuria of >0.5 g/day or >3 g/day on dipstick or cellular casts) 8. Neurologic disorders (seizures or psychosis in the absence of known causes) 9. Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia) 10. Immunologic disorders (antibodies against double-stranded DNA [dsDNA] or Smith [Sm] antigen, false-positive serologic test for syphilis, or antiphospholipid antibodies [anticardiolipin antibody or lupus anticoagulant]) 11. Presence of antinuclear antibody (ANA)

Question 30

Treatment SLE

Answer 30

Mild forms of SLE are treated with nonsteroidal antiinflammatory drugs, such as aspirin, ibuprofen, or naproxen, to reduce inflammation and relieve pain. Low-dose corticosteroids, such as prednisone, are often prescribed with higher doses used for more serious active disease. Antimalarial medications (e.g., hydroxychloroquine) are preferred treatments for individuals with stable disease. Immunosuppressive drugs (e.g., methotrexate, azathioprine, or cyclophosphamide) are used to treat individuals with severe symptoms involving internal organs who have not responded to high-dose corticosteroids. Ultraviolet light can worsen symptoms (known as flares), and protection from sun exposure is helpful. IVIG

Question 31

Universal donor

Answer 31

O. lacks both types of antigens Has anti A and anti B antibodies

Question 32

Universal recipient

Answer 32

AB. Has no antibodies

Question 33

immune deficiency

Answer 33

linical sequelae (results) of impaired function of one or more components of the immune or inflammatory response , failure of these mechanisms of self-defense to function at their normal capacity, resulting in increased susceptibility to infections.

Question 34

primary immune deficiencies

Answer 34

tendency to develop unusual or recurrent, severe infections. The most severe primary immune deficiencies develop in young children 2 years old and younger. Infections are generally recurrent with only short intervals of relative health. ften have eight or more purulent ear infections, two or more serious sinus infections, and two or more pneumonias, recurrent abscesses or infections in unusual sites, or persistent fungal infections within a year. PO ABX ineffective, need IV Result of single gene defects

Question 35

A.C.I.D.

Answer 35

Anaphylactic -1 Cytotoxic-type 2 Immune complex-3 Delayed-4

Question 36

Type1-4 reactions are mediated by:

Answer 36

Type 3 hypersensitivity reactions involve the formation of immune complexes that can deposit in tissues, leading to complement activation and inflammation. This process can cause tissue damage and is associated with systemic lupus erythematosus (SLE) and serum sickness. ​ Type 1 reactions are mediated by IgE antibodies, and type 2 are mediated by IgG or IgM antibodies. Type 4 reactions are activated by T-helper cells.

Question 37

Risk for developing asthma

Answer 37

history of atopic disease (eczema, a form of atopic dermatitis

Question 38

Difference in type 2 and type 3 responses

Answer 38

type 2 response, the antibody binds to the antigen on the cell surface, but in type 3 responses, the antibody binds to the antigen in the blood or body fluids and then circulates to the tissue

Question 39

pathophysiological processes of a type 3 immune complex hypersensitivity in the correct order

Answer 39

Antibodies bind to antigens​ Immune complexes form​ Complexes deposit in blood vessels or tissues​ Activation of complement​ Inflammatory response at the site of deposit​ Release of lysosomal enzymes and chemical mediators​ Tissue damage

Question 40

Acute HIV infection:​

Answer 40

After initial infection, the acute HIV infection stage occurs first, typically 2–3 weeks after infection, characterized by high viral replication and dissemination throughout the body with the client potentially experiencing nonspecific flu-like symptoms as the immune system begins to respond to the virus. RNA retrovirus that primarily infects and destroys CD4+ helper T cells use reverse transcriptase, allowing the virus to copy RNA into DNA and replicate inside the host’s cells

Question 41

Clinical latency

Answer 41

Clinical latency is the second stage of HIV infection, which can last for a year or more. This stage is characterized by low levels of HIV replication and persistent immune activation, with CD4+ helper T cell counts gradually declining. The client may not experience symptoms during this stage.

Question 42

AIDS

Answer 42

AIDS is the final and most severe stage of infection, where the immune system is badly damaged. AIDS is characterized by a CD4+ T cell count below 200 cells/mm3 with the body becoming vulnerable to opportunistic infections, opportunistic malignancies, and neurological complications. Without treatment, survival time averages 3 years.​

Question 43

two types of immunodeficiency disorders:

Answer 43

Primary: genetic or congenital defects, at birth Secondary: HIV, acquired during an individual’s life and caused by a factor external to the immune system

Question 44

Intrinsic Risk Factors

Answer 44

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.

Question 45

Extrinsic Risk Factors

Answer 45

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.

Question 46

Treatment-Related Risk Factors

Answer 46

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.