Immune System Disorders

In which order does the mechanisms of a type IV hypersensitivity occur? - Exposure to causative agent -Release of chemical mediators -Accumulation of macrophages at infection site -Activation of T-cells

- Exposure to causative agent -Activation of T-cells -Release of chemical mediators -Accumulation of macrophages at infection site

The nurse notices the ear canal of a patient is red and inflamed. Which cell would be most active in the first stage of inflammation? -Basophils -Eosinophils - Macrophages -Tissue -mast cells

- Macrophages Rationale: The macrophages are the primary cells that affect the first stage of the inflammatory process. The macrophages secrete cytokines to mature white blood cells faster. Basophils, eosinophils, and tissue mast cells are predominantly active in the second stage of inflammation.

Which immune cell or component is involved in a type IV hypersensitivity reaction? - T-cells -Self cells -Antibodies -Complement

- T-cells Rationale: Type IV hypersensitivity is caused by T-cell mediated reactions. These cells release chemical mediators and activate macrophages to kill antigens. Self cells are present in type II cytotoxic reactions when autoantibodies are produced against these cells. The self cell is then destroyed by phagocytosis. Antibodies and complement play no role in type IV hypersensitivity reactions but do in type Ill immune complex—mediated reactions.

Antigen response needs: (1

- need exposure to occur for antigen to generate a response. Body triggers response to get rid of the invader

Which event occurs in a type II hypersensitivity reaction?

-Immunoglobulin G (IgG) antibody reacts with host cell membrane. Rationale Type II hypersensitivity reactions are also called cytotoxic reactions. The mechanisms involved in type II hypersensitivity reactions include the reaction of the IgG antibody with the host cell membrane or antigen being adsorbed by the host cell membrane. The reaction of the lgE antibody on mast cells with antigen results in the release of mediators, especially histamine. This mechanism is involved in type I hypersensitivity reactions. The reaction of autoantibodies with normal cell-surface receptors stimulates a continual overreaction of the target cell. This mechanism is involved in type V hypersensitivity reactions. The reaction of sensitized T-cells with antigen and the release of lymphokines activate macrophages and induce inflammation. This is the mechanism involved in type IV hypersensitivity reactions

Which mechanism is involved in type II hypersensitivity reaction? - Activation of T-cells -Phagocytosis of self cells -Stimulation of thyroid cells -Secretion of histamines from mast cells

-Phagocytosis of self cells Rationale In type II reactions, an autoantibody is produced against the self cell that contains an antigen or foreign protein on its surface. The self cells are then destroyed by phagocytosis or lysis. Activation of T-cells takes place in delayed hypersensitivity. Stimulation of thyroid cells and secretion of histamines are the mechanisms of type V and type I hypersensitivities, respectively.

Which action takes place during the third stage of inflammation if there is permanent tissue damage that cannot be replaced? -Fluid leaks -Edema occurs -Exudate forms -Scar tissue develops -New blood vessels grow

-Scar tissue develops -New blood vessels grow Rationale: In the third stage of inflammation, the white blood cells cause scar tissue to form and new blood vessels to grow, which completes the healing process. The second stage of inflammation causes fluid to leak, edema to occur, and exudate to form.

Which condition is associated with a type II hypersensitivity reaction? -Hay fever -Sarcoidosis -Serum sickness -Autoimmune -hemolytic anemia

-hemolytic anemia Rationale Hemolytic anemia is a type II hypersensitivity disorder. In this reaction, the body makes special autoantibodies to kill the self cells (or blood cells), causing anemia because of loss of blood cells. Hay fever, serum sickness, and sarcoidosis are type l, type Ill, and type IV hypersensitivities, respectively.

Adaptive Immunity def: (2)-

1. Acquired immunity 2. Protective response that is specific 3. results in long-term resistance to the effects of invading microorganisms

Type 1 hypersensitvity: (3)

1. Aka rapid hypersensitivity, or atopic allergy 2. Most common type 3. From IgE increased production

Anaphylaxis Drug Therapy:

1. Antihistamines (Diphenhydramine (Benadryl)-H1/ Cimetidine (Tagamet) & Ranitidine (Zantac)-H2 2. Leukotriene antagonists or modifiers; Montelukast (singulair)

Systemic Lupus Erythematosus: definition:

1. Chronic/progressive/ AID 2. Tissue integrity is lost via excessive inflammation and overactive immunity leading to organ failure and death

Anaphylaxis Interventions:

1. Establish/stabilize the airway 2. If IV drug is suspected as the cause/discontinue 3. Call RRT 4. Apply 02 5. Prepare to admin epi for anaphylaxis, diphenhydramine for angioedema/uticaria 6. Other interventions depend on degree of problem

Phaygocytosis-stages (7)

1. Exposure/invasion 2. Attraction 3. Adherence 4. Recognition 5. Cellular ingestion 6. Phagosome formation 7. degradation

General Autoimmunity:

1. Inappropriate immunity develops to an adult's own tissues 2. In response, the body's antibodies or lymphocytes are directed against the body's own healthy, normal cells and tissues (not just against invaders) 3. Autoimmune disorders are common, chronic, progressive, self-perpetuating

Type 1 hyper sensitivity allergic reaction from (4):

1. Inhaled (plant pollens, fungal spores, animal dander, house dust, grass, ragweed) 2. Ingested (foods, food additives, drugs) 3. Injected (insect or other venom, drugs, biologic substances such as contrast dyes) 4. Skin or mucous membrane contacted (latex, pollens, foods, environmental proteins)

Anaphylaxis Assessment: Recognize these Signs & Symptoms

1. Initial symptoms are subtle 2. Apprehension/weakness/impending doom 3. Respiratory symptoms 4. Hypotension 5. Diaphoresis

Cell mediated immunity is (4):

1. Natural Immunity: Provides a nonspecific response to foreign pathogen (present at birth/rapid) 2. Maintains a broad spectrum of defense 3. The basis of this defense is the ability to distinguish between "self" and "non-self" 4. Aided by both the inflammatory & immune response systems

Anaphylaxis: type of reaction

1. Type 1 hypersensitivity 2. Rapid/systemic 3. Can be fatal

Degree of allergic reaction ranges from: (2

1. Uncomfortable (wheezing/watery eyes/ sneezing 2. Life threatening (allergic asthma, angioedema, anaphylaxis, bronchoconstriction, circulatory collapse)

Type III Immune Complex Reactions are from; 2

1. from excess antigens causing immune complexes to form in the blood 2. Most autoimmune disorders are caused by this type of reaction

Inflammation is; 4:

1. innate-native immunity or natural immunity (1st line) 2. Provides immediate protection against effects of tissue injury and foreign proteins 3. Non-specific 4. Part of gen immunity

Angioedema background

1. severe type 1 sensitivity: 2. Involves all blood vessels/skin layers/mucus membranes/sub q layers 3. Lips,, face, tongue, larynx, neck 4. ACEIs for HTN

Cell types involved in inflammation

1.Neutrophils: 2. Macrophages: 1st to cite 3. Basophils: 4. Eosinophils: 5: Tissue Mast Cells

Sequence of inflammatory responses (3)

1: vascular—change in blood vessels; redness and warmth (as evidence by—diagnosis) Stage 2. cellular exudate—neutrophilia, pus Stage 3. tissue repair and replacement —WBCs trigger new blood vessel and growth and scar tissue formation

Agglutination (4):

1: when antibody binds to antigen 2-links (chains of immune complexes) 3. eliminate or neutralize the bound antigen 4. hopefully leads to destruction of invading cells

antibody classifications

5 types classified by: size, location, amount, and function

Which happens during stage 2 of the inflammatory process: 1. neutrophils attach/destroy 2. edema forms at the site 3. increased blood flow to injured area 4. increased # of neutrophils circulating 5. Pus with WBS/necrotic tissue/fluids

Correct: 1. neutrophils attach/destroy 4. increased # of neutrophils circulating 5. Pus with WBS/necrotic tissue/fluids

Which white blood cell type does the nurse expect to be most active in a patient who presents to the emergency department with roundworm, a parasitic infestation?

Eosinophils

Which substance is released in the first stage of inflammation? Select all that apply, One, some, or all responses may be correct: -Kinins -Serotonin -Histamine -Chemotaxins -Cyclooxygenas

Kinins, serotonin, and histamine Rationale Kinins, serotonin, and histamine are released in the first stage of inflammation. Damaged tissues secrete chemotaxins that attract neutrophils and macrophages. Cyclooxygenase is released in the second stage of inflammation.

Which inflammatory condition is caused by an infection? Meningitis Pneumonia Joint sprain Myocardial infarction Blister formation

Meningitis Pneumonia Rationale:Examples of inflammation without infection include joint sprains, myocardial infarction, and blister formation. Meningitis is inflammation of the meninges, and pneumonia is inflammation of the lung parenchyma; both conditions are caused by an infection

Which two cells of the immune system engulf foreign cells through phagocytosis?

Neutrophils and macrophages

The nurse recalls that which condition is an example of inflammation from infection? Otitis media Blister formation Allergic rhinitis Myocardial infarction

Otitis media Rationale: Examples of inflammation from infection include otitis media, appendicitis, and viral hepatitis, among many others. Myocardial infarction is associated with inflammation. However, this inflammation is not caused by infection. Blister formation is an example of inflammation that occurs without infection. Allergic rhinitis is an example of inflammation that occurs from the invasion of noninfectious microorganisms.

Hypersensitivities/Allergies definition:

Overactive immunity with excessive inflammation in response to presence of an antigen to which patient has been previously exposed

Which is a common trigger for allergic rhinitis? Select all that apply. -Hay fever Latex gloves Plant pollen Animal dander Dust and molds

Plant pollen Animal dander Dust and molds Rationale Allergic rhinitis, or hay fever, is triggered by immunity and inflammatory reactions to airborne allergens, especially plant pollen, molds, dust, animal dander, wool, food, and air pollutants. Latex products are not associated with allergic rhinitis.

Which is a key function of Basophils?

Release histamine and heparin in areas of tissue damage.

Which is a key function of eosinophils?

Release vasoactive amines during allergic reactions.

Which stage of inflammation is occurring when a patient with an ingrown toenail experiences redness, pain, and pus exudate when pressure is placed on the toe?

Stage 2: Rationale: The presence of pus is a classic sign of stage II of the inflammatory process. Edema occurs in stage l, but this does not reflect true pus formation. Pus formation occurs when the body rids itself of dead white blood cells, necrotic tissue, and fluids during stage II. Stage Ill is the healing stage, and pus formation is usually no longer occurring during this stage. The inflammatory process does not include a stage IV.

Type IV Delayed Hypersensitivity: (5):

T-lymphocytes (T-cells) are the activated immune system component triggering the excessive responses

Which of the following information should be included when providing an education about the healing process involved with myocardial infarctions? The heart muscle is a nondividing tissue. -White blood cells (WBCs) trigger new blood vessel growth. -The heart muscle regains its effectiveness. -Scar tissue contracts like the heart tissue. -Scar tissue prevents the formation o fa hole in the muscle wall as ischemic cells die.

The heart muscle is a nondividing tissue. -White blood cells (WBCs) trigger new blood vessel growth. -Scar tissue prevents the formation o fa hole in the muscle wall as ischemic cells die. The heart is nondividing tissue. When a myocardial infarction occurs, WBCs trigger new blood vessel growth and scar tissue formation. Scar tissue prevents the formation of a hole in the muscle. Scar tissue also replaces the heart muscle destroyed because of a myocardial infarction. The effectiveness of the left ventricular contraction is reduced. Scar tissue only serves as a patch; it does not contract or serve as heart muscle.

Type of reaction where: sensitized T-cells from previous exposure respond to an antigen by releasing chemical mediators and triggering macrophages to destroy the antigen

Type IV reaction (delayed hypersensitivity reactions),

How acquire innate immunity

We're born with it

Antibidoy -mediated immunity:

different receptors—don't get hung up on this

B-lymphocytes changes:

take longer to become sensitized/begin to make antibodies to new antigen exposures (this is bad bc response is longer)

The development of a poison ivy skin rash is an example of a

type IV reaction.

-Sarcoidosis

type Ill

Type 1 hyper: Anaphylaxis (medical emergency):

1. Blood vessel dilation 2. Decreased cardiac output 3. Bronchoconstriction

SLE Lab assessment:

1. ESR 2. Serum complement levels for C3 and C4 3. ANAs (antinuclear antibody) 4. Other diagnostic assessment 5. Blood and urine tests

SLE Psychosocial Assessment:

1. Fear 2. Anxiety 3. Assess disorder feelings 4. Determine usual coping mechanisms/support systems

Protection Provided by CMI 2:

1. Helps protect body through ability to differentiate self from non-self 2. Prevents development of cancer and metastasis after exposure to carcinogens

Angioedema History: drugs, esp for HBP: 1. Angioedema Physical Assessment: (4):

1. Lip swelling, itching in back of throat 2. Deep, firm swelling of face, lips, tongue neck 3. Difficulty speaking, drinking 4. Nasal swelling

SLE Planning Implementation:

1. Managing persistent pain 2. Managing fatigue 3. Preventing organ failure and reducing SLE activity periods 4. Enhancing self-esteem

Infection: 4 steps

1. Pathogens invade body 2. Triggers inflammation 3. Inflammation can occur without infection 4. Infection usually triggers inflammation

SLE Analysis: Analyze cues/prioritize hypotheses

1. Persistent pain (chronic inflammation/hypoxia from vasculitis-in tissues/organs 2. Fatigue (inflammation/hypoxia-esp during flares 3. Potential tissue loss/organ failure 4. Decreased self-esteem bc body image changes from d/o progression/therapy

Natural immunity: 3

1. Phys/chem barriers 2. Physical 3. Chemical

Anaphylaxis: health promotion/maintenance:

1. Prevention is best (avoid allergens/wear bracelet/tell healthcare about allergies 2. Carry epi/anaphylaxis injector 3. Health records should display specific allergens 4. Implement precautionary measures if drug or agent must be used despite history of allergic reaction

Angioederma Interventions:

1. Stop reaction 2. Ensure adequate airway 3. 02 intubation/tracheostomy/drug therapy

SLE etiology & genetic risk:

1. Strong genetic connection 2. Triggers: infection, injury, drugs, hormones, exposure

SLE Evaluate outcomes:

1. Understand the basis of the disorder and its management 2. Accept the life-style changes needed to protect herself or himself to prevent complications 3. Be an active partner in the prescribed long-term SLE management plan 4. Have pain levels reduced to the extent that she or he can participate in job-related, family, and social activities to a degree acceptable to her or him 5. Have reduced number and severity of flares and longer periods of remission with low SLE activity. 6. Remain free from infection 7. Express a positive perception of herself or himself

5 signs of inflammation

1. Warmth 2. Redness (erythemia) 3. Swelling 4. Pain (doc on scale, OLD CARTS, faces scale (Wong Vapor)) 5. Decreased function (tells you infection going on/trauma—further investigate

What is the function of leukocytes:

1. destroy foreign invaders 2. help with complement activation 3. produce antibodies against invaders 4. Help recognize self vs non-self

Systemic Lupus Erythematosus: Care Coordination and Transition Management:

1. home care mgmt. 2. self mgmt. education 3. health care resources

Systemic Lupus Erythematosus: Physical Assessment: S & S:

1.Red, macular, facial rash ("butterfly") 2. Discoid rash - face, scalp, sun-exposed areas 3. Photosensitivity 4. Chronic lesions on mucous membranes 5. Nonerosive arthritis 6. Serosal membrane inflammation 7. Neurologic, hematologic, immunity problems 8. ANAs

SLE Physical Assessment:

1.Skin: urticaria -> acute or chronic response 2. Infection: Fever! 3. Lymph Nodes: palpate for enlargement -> activation against pathogens 4. Joints: inflammation and infiltration of leukocytes

Immunity in the older adult affected by: (5)

1: Nutrition status, environmental conditions, drug, disease, and age change immunity 2: Microbiome changes (overgrowth of more pathogenic organisms) 3:Lower T-cell function (normally they help w/inflammation and allergic reactions) 4: B-lymphocytes: take longer to become sensitized/begin to make antibodies to new antigen exposures (this is bad bc response is longer) 5; Circulating autoantibodies increase: (why dev. Auto immune illnesses overtime)

Which is an example of a type I hypersensitivity reaction? Angioedema Rheumatoid arthritis Poison ivy skin rashes Immune hemolytic anemia

Angioedema Type I hypersensitivity reactions are caused by overactive immunity and result from increased production of immunoglobulin E. Examples of type I reactions include angioedema, anaphylaxis, and allergic asthma. Rheumatoid arthritis is an example ofa type Ill hypersensitivity reaction

types of acquired antibody mediated immunity

Antibody classifications

which immune cell is highly active during a type I hypersensitivity reaction?

Basophils Rationale: Basophils are highly reactive during allergic and hypersensitivity reactions because of the presence of immunoglobulin E (lgE) on their surfaces. Monocytes are relatively inactive and are not usually involved in hypersensitivity reactions. Although neutrophils and macrophages may play a role in hypersensitivity because of the general inflammatory response, their role is not as prominent as the role of basophils in this process.

For total or full immunity

CMI must function optimally

Which is a key function of neutrophils?

Help in nonspecific ingestion and phagocytosis of microorganisms.

Which is a key function of Macrophages?

Help in recognition of foreign proteins and microorganisms.

Which antibody level increases during type I hypersensitivity allergy?

IgE In a patient exposed to an allergen, elevated levels of immunoglobulin E (lgE) antibodies are produced. The elevated levels of antibodies cause inflammation, erythema, or edema in the affected region.

larges amount of antibodies are:

IgG

Which food item may cause anaphylaxis in some individuals? Select all that apply. One, some, or all responses may be correct. Nuts Eggs Peanuts Shellfish Potatoes

Nuts Eggs Peanuts Shellfish

T-cell function changes

normally they help w/inflammation and allergic reactions

Microbiome changes

overgrowth of more pathogenic organism's

Lyme Disease: If untreated

progresses to Stage II, and III

Immunity:

protection from illness or disease that is maintained by the body's physiologic defense mechanisms.

Sensitized T-cells (from a previous exposure) respond to an antigen by

releasing chemical mediators and triggering macrophages to destroy the antigen.

Lyme Disease Cause:

spirochete Borrelia burgdorferi

Antibodies and complement are not involved in this type of reaction:

type 4

IgG antibodies play a crucial role in

type II allergies.

Immune hemolytic anemia is a form of

type II reaction (cytotoxic reaction), which occurs when the body makes autoantibodies directed against the body's own cells.

-Serum sickness

type IV

Type of reaction where: excess antigens cause immune complexes to form in the blood, and these circulating complexes lodge themselves in the small blood vessels of the kidneys, skin, and joints.

type Ill hypersensitivity reactions (immune complex reactions)

-Hay fever

type l

Acquired immunity

vaccines

Microbiome -

all microorganisms of normal flora that coexist in and on a person

Lyme Disease Immediately remove

any ticks

WBC: active during hypersensitivity reaction

basophils, because of IgE on their surfaces

Lyme Disease Result:

chronic inflammation

Organization of the Immune system

immune system, stem cells, leukocytes

Older adult patho changes in

immunity, inflammation, pt care with hypersensitivity (allergy)/immunity

all antibodies are

immunoglobins

Eosinophils;

inflammation/allergic reactions/ asthmatic reactions—can affect eosinophil

Antigen-antibody interactions (2 steps):

(1) Antigen recognition - recognition of antigen by unsensitized B-cells 2). Sensitization - occurs when B-cell recognizes the antigen as non-self and is now "sensitized" to this antigen

Which is the name of the process used to make antigens less likely to grow in the body, thus making them effective for immunizations?

Attenuation

Which medication is most likely to have caused a hypersensitivity reaction of severe angioedema of the lips, face, and tongue? Acarbose Asenapine Benazepril Gabapentin

Benazepril Rationale The drugs most commonly associated with angioedema are angiotensin-converting enzyme inhibitors, such as benazepril. Acarbose is a diabetic medication. Asenapine is an atypical antipsychotic. Gabapentin is an anticonvulsant

Type II Cytotoxic Reactions is where:

Body makes autoantibodies directed against self cells that have some form of foreign protein attached to them

Hypersensitivy type 2 reactions are

Cytotoxic Reactions

Which is the function of a monocyte during inflammation?

Destruction of bacteria and cellular debris

Which is the function of a monocyte during inflammation?

Destruction of bacteria and cellular debris. Rationale: During inflammation, monocytes destroy bacteria and cellular debris. Basophils releases histamine and heparin in areas of tissue damage. The function of neutrophils is nonspecific ingestion and phagocytosis of microorganisms. The function of macrophages is nonspecific recognition of foreign proteins and microorganisms.

Which symptom is associated with an anaphylactic reaction?

Red blotches, itching, urticaria, erythema, and angioedema

SLE Incidence:

SLE Incidence: 1,6 mil adults in US

SLE prevalence:

SLE prevalence: 5 mil ww

In which stage of inflammation is there an increased number of circulating neutrophils and exudate formed?

Stage 2: Rationale: During stage II of inflammation, there is an increased number of circulating neutrophils and exudate formed. Stage I is characterized by a vascular response that starts the changes in blood vessels. Stage Ill features tissue repair and replacement.

Occurs hours to days after exposure

Type 4

Cell-mediated immunity involves:

WBC actions/interactions

Type 1 hyper: Five cardinal signs of inflammation

Warmth, Redness, Swelling, Pain, Decreased function

Inflammation

a syndrome of normal tissue responses to cellular injury, allergy, pathogen presence

Lyme Disease Stage I

flu-like symptoms, bull's eye rash

Lyme Disease Avoidance of/use:

heavily wooded areas is best prevention; use insect-repellent; wear long-sleeved tops and long pants

Which type of hypersensitivity is cell-mediated immunity with T-lymphocyte as the reactive cell?

Delayed hypersensitivity Rationale Type IV hypersensitivity is a type of cell-mediated response that is often called delayed type hypersensitivity, because the reaction takes 2 to 3 days to develop.

Type IV : reaction signs:

Edema, induration, ischemia, tissue damage at site of exposure (e.g., dermatitis)

why dev. Auto immune illnesses overtime

Circulating autoantibodies increase