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Med Surg II > Exam 1: Ch 50, 51, 52, 53 > Flashcards

Exam 1: Ch 50, 51, 52, 53 Flashcards

1
Q

agglutination

A

clumping effect occurring when an antibody acts as a cross-link between two antigens.

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2
Q

antibody

A

Is a large protein, called an immunoglobulin, that consists of two subunits, each containing a light and a heavy peptide chain held together by a chemical link composed of disulfide bonds. Each subunit has one portion that serves as a binding site for a specific antigen and another portion that allows the antibody molecule to take part in the complement system.

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3
Q

antigen

A

substance that induces the production of antibodies

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4
Q

antigenic determinant

A

the specific area of an antigen that binds with an antibody combining site and determines the specificity of the antigen-antibody reaction

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5
Q

apoptosis

A

programmed cell death that results from the digestion of deoxyribonucleic acid by endonucleases.

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6
Q

B cells

A

Cells that are important for procuring a humoral immune response

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7
Q

Cellular immune response

A

the immune system’s third line of defense, involving the attack of pathogens by T cells

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8
Q

Complement

A

series of enzymatic proteins in the serum that, when activated, destroy bacteria and other cells

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9
Q

Cytokines

A

generic term for non-antibody proteins that act as intercellular mediators, as in the generation of immune response.

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10
Q

Cytotoxic T cells

A

lymphocytes that lyse cells infected with virus; also play a role in graft rejection.

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11
Q

Epitope

A

any component of an antigen molecule that functions as an antigenetic determinant by permitting the attachment of certain antibodies.

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12
Q

helper T cells

A

lymphocytes that attack foreign invaders (antigens) directly

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13
Q

Humoral immune response

A

the immune system’s second line of defense; often termed the antibody response

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14
Q

Immune response

A

the coordinated response of the components of the immune system to a foreign agent or organism

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15
Q

Immune system

A

the collection of organs, cells, tissues, and molecules that mediate the immune response.

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16
Q

Immunity

A

the body’s specific protective response to a foreign agent or organism; resistance to disease, specifically infectious diseases.

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17
Q

Immunopathology

A

study of diseases resulting in dysfunctions within the immune system.

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18
Q

Immunoregulation

A

complex system of checks and balances that regulates or controls immune responses

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19
Q

Interferons

A

proteins formed when cells are exposed to viral or foreign agents; capable of activating other components of the immune system

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20
Q

Lymphokines

A

substances released by sensitized lymphocytes when they come in contact with specific antigens

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21
Q

Memory Cells

A

cells that are responsible for recognizing antigens from previous exposure and mounting an immune response.

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22
Q

Natural killer (NK) cells

A

lymphocytes that defend against microorganisms and malignant cells.

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23
Q

Null lymphocytes

A

lymphocytes that destroy antigens already coated with the antibody.

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24
Q

Opsonization

A

The coating of antigen-antibody molecules with a sticky substance to facilitate phagocytosis.

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25
Q

Phagocytic cells

A

cells that engulf, ingest, and destroy foreign bodies or toxins

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26
Q

Phagocytic immune response

A

the immune system’s first line of defense, involving white blood cells that have the ability to ingest foreign particles

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27
Q

Stem cells

A

precursors of all blood cells; reside primarily in bone marrow

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28
Q

suppressor T cells

A

lymphocytes that decrease B-cell activity to a level at which the immune system is compatible with life

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29
Q

T cells

A

cells that are important for producing a cellular immune response.

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30
Q

Immune function is affected by a variety of factors such as:

A 
central nervous system integrity
general physical and emotional status
medications
dietary patterns
stress of illness, trauma, or surgery
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31
Q

Immune memory is:

A

a property of the immune system that provides protection against harmful microbial agents despite the timing of re-exposure to the agent.

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32
Q

Disorders of the immune system may stem from:

A
  • excesses or deficiencies of immunocompetent cells
  • alterations in the function of these cells
  • immunologic attack on self-antigens
  • inappropriate or exaggerated responses to specific antigens
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33
Q

Autoimmunity

A

normal protective immune response paradoxically turns against or attacks the body, leading to tissue damage

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34
Q

Hypersensitivity

A

body produces inappropriate or exaggerated responses to specific antigens

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35
Q

Gammopathies

A

Immunoglobulins are overproduced

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36
Q

Primary immune deficiencies

A

deficiency results from improper development of immune cells or tissues; usually congenital or inherited

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37
Q

Secondary immune deficiencies

A

Deficiency results from some interference with an already developed immune system; usually acquired later in life

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38
Q

The major components of the immune system include:

A 
central and peripheral organs, tissues, and cells:
Adenoids/Tonsils
Thymus
Bronchus-associated lymphoid tissue
Axillary lymph nodes
Spleen
Intestine
Peyer's patches
Appendix
Inguinal lymph nodes
Bone marrow (B cells and T cells)
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39
Q

Bone marrow

A

WBCs involved in immunity are produces in the bone marrow.
Lymphocytes are generated from stem cells.
2 types of lymphocytes: B cells and T cells
B cells: mature in the bone marrow then enter circulation
T cells: move from the bone marrow to the thymus, where they mature into several kinds of cells with different functions.

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40
Q

Lymphoid tissues

A

Lymph nodes, spleen, blood, and lymph

  • Spleen: red/white pulp; acts as a filter. Red pulp is site where RBCs are destroyed. White pulp contains concentrations of lymphocytes.
  • Lymph Nodes: remove foreign material from the lymph system before it enters the bloodstream. They also serve as centers for immune cell proliferation.
  • Remaining lymphoid tissues contain immune cells that defend the body’s mucosal surfaces against microorganisms.
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41
Q

The basic function of the immune system is to:

A

remove foreign antigens such as viruses and bacteria to maintain homeostasis.

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42
Q

There are 2 general types of immunity:

A
  1. natural (innate) immunity-present at birth

2. acquired (adaptive) immunity-develops after birth

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43
Q

Natural immunity

A
  • Is nonspecific
  • provides broad spectrum of defense against and resistance to infection
  • first line of host defense following antigen exposure, because it protects the host “without remembering” prior contact with an infectious agent.
  • co-coordinates the initial response to pathogens through the production of cytokines and other effector molecules.
  • cells involved include macrophages, monocytes, dendritic cells, NK cells, basophils, eosinophils, and granulocytes.
  • the early events in this process are critical in determining the nature of the adaptive immune response.
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44
Q

Natural immune mechanisms can be divided into two stages:

A

Immediate: occurring within 4 hours
Delayed: occurring between 4 and 96 hours after exposure

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45
Q

White Blood Cell Action

A

-WBC’s or leukocytes, participate in both the natural and the acquired immune responses.
Granulocytes fight invasion by foreign bodies or toxins by releasing cell mediators, such as histamine, bradykinin, and prostaglandins, and engulfing the foreign bodies or toxins.
-Granulocytes include neutrophils, eosinophils, and basophils.

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46
Q

Neutrophils

A

are the 1st cells to arrive at the site where inflammation occurs.

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47
Q

Eosinophils and basophils increase in number during

A

allergic reactions and stress responses.

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48
Q

Monocytes function as

A

phagocytic cells, engulfing, ingesting, and destroying greater numbers and quantities of foreign bodies or toxins than granulocytes do.

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49
Q

60-70% of lymphocytes in the blood are

A

T cells

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50
Q

10 to 20% of lymphocytes in the blood are

A

B cells

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51
Q

The inflammatory response is a major function of the natural immune system that is elicited in response to

A

tissue injury or invading organisms.

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52
Q

Chemical mediators assist in the inflammatory response by:

A 
minimizing blood loss
walling off the invading organism
activating phagocytes
promoting formation of fibrous scar tissue 
regeneration of injured tissue
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53
Q

Physical surface barriers include:

A

intact skin
mucous membranes
cilia of the respiratory tract

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54
Q

Chemical barriers

A 
mucus
acidic gastric secretions
enzymes in tears and saliva
wax
sweat
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55
Q

If an immune response fails to develop and clear an antigen sufficiently, the host is considered to be:

A

Immunocompromised or immunodeficient

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56
Q

If immune regulation is overtly robust or misdirected, the following may result:

A

allergies
asthma
autoimmune disease

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57
Q

Most microbial infections induce an inflammatory response mediated by:

A

T cells and cytokines, which, in excess, can cause tissue damage.

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58
Q

The acquired immune response is broadly divided into two mechanisms:

A
  1. the cell-mediated response, involving T-cell activation

2. effector mechanisms, involving B-cell maturation and production of antibodies.

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59
Q

Active acquired immunity

A

refers to immunologic defenses developed by the person’s own body. This immunity typically lasts many years or even a lifetime.

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60
Q

Passive acquired immunity

A

is temporary immunity transmitted from a source outside the body that has developed immunity through previous disease or immunization.

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61
Q

When the body is invaded or attacked by bacteria, viruses, or other pathogens, it has 3 means of defense?

A
  1. the phagocytic immune response
  2. the humoral or antibody immune response
  3. the cellular immune response
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62
Q

1st line of defense

A

The phagocytic immune response, primarily involves WBCs, which have the ability to ingest foreign particles and destroy the invading agent

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63
Q

2nd protective response

A

Humoral immune response (sometimes called the antibody response), begins with the B lymphocytes, which can transform themselves into plasma cells that manufacture antibodies. These antibodies are highly specific proteins that are transported in the bloodstream and attempt to disable invaders.

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64
Q

3rd mechanism of defense

A

The cellular immune response, also involved T-lymphocytes, which can turn into special cytotoxic (or killer) T cells that can attack the pathogens.

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65
Q

The structural part of the invading or attacking organism that is responsible for stimulating antibody production is called an:

A

antigen (or an immunogen)

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66
Q

There are four well-defined stages in an immune response:

A

recognition, proliferation, response, and effector.

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67
Q

Recognition stage of an immune response

A
  • recognition of antigens as foreign, or non-self, by the immune system is the initiating event in any immune response.
  • it involves the use of lymph nodes and lymphocytes for surveillance
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68
Q

Proliferation stage of an immune response

A
  • the circulating lymphocytes containing the antigenic message return to the nearest lymph node
  • once in the node, these sensitized lymphocytes stimulate some of the resident T and B lymphocytes to enlarge, divide, and proliferate.
  • T lymphocytes differentiate into cytotoxic (or killer) T cells, whereas B lymphocytes produce and release antibodies.
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69
Q

Response stage of an immune response

A
  • the differentiated lymphocytes function in either a humoral or a cellular capacity.
  • this stage begins with the production of antibodies by the B lymphocytes in response to a specific antigen
  • the cellular response stimulates the resident lymphocytes to become cells that attack microbes directly rather than through the action of antibodies. These transformed lymphocytes are known as cytotoxic (killer) T cells.
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70
Q

Viral antigens induce a _________ response.

A

Cellular.
-This response is manifested by the increasing number of T lymphocytes seen in the blood tests of people with viral illnesses such as infectious mononucleosis.

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71
Q

Effector stage of an immune response

A
  • either the antibody of the humoral response of the cytotoxic (killer) T cell of the cellular response reaches and connects with the antigen on the surface of the foreign invader.
  • This initiates activities involving interplay of antibodies, complement, and action by the cytotoxic T cells.
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72
Q

Humoral immune response

A

Is characterized by the production of antibodies by B lymphocytes in response to a specific antigen.

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73
Q

Antigen recognition

A
  • B lymphocytes recognize and respond to invading antigens in more than one way.
  • B lymphocytes respond to some antigens by directly triggering antibody formation; however, in response to other antigens, they need the assistance of T cells to trigger antibody formation
  • with the help of macrophages, the T lymphocytes are believed to recognize the antigen of a foreign invader
  • Memory cells are responsible for the more exaggerated and rapid immune response in a person who is repeatedly exposed to the same antigen.
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74
Q

Humoral Responses (B cells)

A
  • bacterial phagocytosis and lysis
  • anaphylaxis
  • allergic hay fever and asthma
  • immune complex disease
  • bacterial and some viral infections
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75
Q

Cellular responses (T cells)

A
  • transplant rejection
  • delayed hypersensitivity (tuberculin reaction)
  • graft-versus-host disease
  • tumor surveillance or destruction
  • intracellular infections
  • viral, fungal, and parasitic infections
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76
Q

Role of antibodies

A
  • Defend against foreign invaders in several ways, and the type of defense used depends on the structure and composition of both the antigen and the immunoglobulin.
  • The antibody molecule has at least two combining sites, or Fab fragments.
  • antibodies promote the release of vasoactive substances, such as histamine and slow-reacting substances, two of the chemical mediators of the inflammatory response.
  • antibodies do not function in isolation; rather, they mobilize other components of the immune system to defend against the invader.
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77
Q

Immunoglobulins

A
  • The body can produce 5 different kinds
  • IgA, IgD, IgE, IgG, and IgM
  • classification is based on the chemical structure and biologic role of the individual immunoglobulin
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78
Q

IgG

A
  • 75% of total immunoglobulin
  • appears in serum and tissues (interstitial fluid)
  • assumes a major role in bloodborne and tissue infections
  • activates the complement system
  • enhances phagocytosis
  • crosses the placenta
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79
Q

IgA

A
  • 15% of total immunoglobulin
  • appears in body fluids (blood, saliva, tears, breast milk, and pulmonary, gi, prostatic, and vaginal secretions)
  • protects against respiratory, gi, and gu infections
  • prevents absorption of antigens from food
  • passes to neonate in breast milk for protection
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80
Q

IgM

A
  • 10% of total immunoglobulin
  • appears mostly in intravascular serum
  • appears as the 1st immunoglobulin produced in response to bacterial and viral infections
  • activates the complement system
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81
Q

IgD

A
  • 0.2% of total immunoglobulin
  • appears in small amounts in serum
  • possibly influences B-lymphocyte differentiation, but role is unclear
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82
Q

IgE

A
  • 0.004% of total immunoglobulin
  • appears in serum
  • takes part in allergic and some hypersensitivity reactions
  • combats parasitic infections
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83
Q

The portion of the antigen involved in binding with the antibody is referred to as the:

A

antigenic determinant

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84
Q

The most efficient immunologic responses occur when the antibody an antigen fit like:

A

a lock and key.

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85
Q

Cross-reactivity

A

-Poor fit can occur with an antibody that was produced in response to a different antigen
-This phenomenon is known as cross-reactivity
Ex: strep and heart valve damage

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86
Q

Cellular Immune Response

A
  • T lymphocytes are primarily responsible for cellular immunity
  • stem cells continuously migrate from the none marrow to the thymus gland, where they develop into T cells
  • despite partial degeneration of the thymus gland that occurs at puberty, T cells continue to develop here.
  • T cells attack foreign invaders directly rather than by producing antibodies.
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87
Q

Types of T Lymphocytes

A
  • T cells include effector T cells, suppressor T cells, and memory T cells.
  • The two major categories of effector T cells are helper T cells and cytotoxic T cells; they participate in the destruction of foreign organisms
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88
Q

Helper T cells

A
  • Are activated on recognition of antigens and stimulate the rest of the immune system.
  • When activated, they secret cytokines, which attract and activate B cells, cytotoxic T cells, NK cells, macrophages, and other cells of the immune system.
  • They also produce lymphokines, one category of cytokines
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89
Q

Cytotoxic T Cells

A
  • Killer T cells
  • attack the antigen directly by altering the cell membrane and causing cell lysis and by releasing cytolytic enzymes and cytokines.
  • Lymphokines can recruit, activate, and regulate other lymphocytes and EBCs.
  • these cells then assist in destroying the invading organism.
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90
Q

Suppressor T cells

A

-have the ability to decrease B-cell production, thereby keeping the immune response at a level that is compatible with health.

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91
Q

Memory cells

A

are responsible for recognizing antigens from previous exposure and mounting an immune response.

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92
Q

Null Lymphocytes

A
  • along with NK cells, are other lymphocytes that assist in combating organisms.
  • These cells are distinct from B cells and T cells and lack the usual characteristics of those cells.
  • Null lymphocytes are a subpopulation of lymphocytes and destroy antigens already coated with antibody.
  • antibody-dependent, cell-mediated cytotoxicity.
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93
Q

Complement

A
  • circulating plasma proteins, known as complement, are made in the liver and activated when an antibody connects with its antigen.
  • plays an important role in the defense against microbes.
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94
Q

Destruction of invading or attacking organisms or toxins is not achieved merely by the binding of the antibody and antigens….

A

It also requires activation of complement, the arrival of killer T cells, or the attraction of macrophages.

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95
Q

Complement has 3 major physiologic functions:

A
  1. defending the body against bacterial infection
  2. bridging natural and acquired immunity
  3. disposing of immune complexes and the byproducts associated with inflammation
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96
Q

The complement cascade

A
  • the proteins that comprise complement interact sequentially with one another in a cascading effect
  • the cascade is important to modifying the effector arm of the immune system
  • activation of complement allows important events, such as removal of infectious agents and initiation of the inflammatory response, to take place.
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97
Q

The complement cascade may be activated by any of three pathways:

A

Classic: triggered after antibodies bind to microbes or other antigens and is part of the humoral type of adaptive immunity.
Lectin: is activated when a plasma protein binds to terminal mannose residue on the surface glycoproteins of microbes.
Alternative: triggered when complement proteins are activated on microbial surfaces; this pathway is part of natural immunity.

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98
Q

Interferons have

A

antiviral and antitumor properties

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99
Q

Interleukin-5 (IL-5)

A

Stimulates the growth and survival of eosinophils and basophils.

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100
Q

Stem cell factor and IL-3

A

Serve as stimuli for multiple hematopoietic cell lines

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101
Q

Assessment of the Immune System

A
  • begins during the health history and physical examination
  • areas to assess include nutritional status, infections and immunizations, allergies, disorders and disease states, surgeries, medications, blood transfusions.
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102
Q

Vitamin D deficiency has been associated with

A
  • increased risk of common cancers
  • autoimmune diseases
  • infectious diseases
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103
Q

Autoimmune disorders

A

-are the 5th leading cause of death by disease in females of reproductive age.

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104
Q

Agammaglobulinemia

A

Disorder marked by an almost complete lack of immunoglobulins or antibodies

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105
Q

Angioneurotic edema

A

Condition marked by development of urticarial and an edematous area of skin, mucous membranes, or viscera.

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106
Q

Ataxia

A

Loss of muscle coordination

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107
Q

Ataxia-telangiectasia

A

Autosomal recessive disorder affecting T-and B-cell immunity primarily seen in children and resulting in a degenerative brain disease

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108
Q

Hypogammaglobulinemia

A

lack of one or more of the five immunoglobulins; caused by B-cell deficiency

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109
Q

Immunocompromised host

A

Person with a secondary immunodeficiency and associated immunosuppression

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110
Q

Panhypoglobulinemia

A

General lack of immunoglobulins in the blood

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111
Q

Severe combined immunodeficiency disease (SCID)

A

Disorder involving a complete absence of humoral and cellular immunity resulting from an x-linked or autosomal genetic abnormality

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112
Q

Telangiectasia

A

vascular lesions caused by dilated blood vessels

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113
Q

Thymic hypoplasia

A

T-cell deficiency that occurs when the thymus gland fails to develop normally during embryogenesis; also known as DiGeorge syndrome

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114
Q

Wiskott-Aldrich syndrome:

A

Immunodeficiency characterized by thrombocytopenia and the absence of T and B cells

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115
Q

Immunodeficiency disorders may be caused by :

A

-a defect in or a deficiency of phagocytic cells, B lymphocytes, T lymphocytes, or the complement system

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116
Q

Regardless of the underlying cause, the cardinal symptoms of immunodeficiency include:

A
  • chronic or recurrent and severe infections
  • infections caused by unusual organisms or by organisms that are normal body flora
  • poor response to standard treatment for infections
  • chronic diarrhea
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117
Q

Primary immunodeficiencies

A
  • the majority are diagnosed in infancy, with a male-to-female ratio of 5 to 1.
  • To date more than 120 immunodeficiencies of genetic origin have been identified.
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118
Q

Clinical manifestations in phagocytic cell disorders

A

-increased incidence of bacterial and fungal infections caused by organisms that are normally nonpathogenic

119
Q

B-cell Deficiencies - Inherited

A

Type 1: results from lack of differentiation of B-cell precursors into mature B cells. This syndrome is x-linked agammaglobulinemia (Bruton’s disease); all the antibodies disappear from the patient’s plasma.
Type 2: results from a lack of differentiation of B cells into plasma cells. Only diminished antibody production occurs with this disorder. This syndrome is called hypogammaglobulinemia and is a frequently occurring immunodeficiency. This is also called CVID.

120
Q

CVID

A
  • the most common primary immunodeficiency seen in adults
  • can occur in people of either gender
  • Most patients are diagnosed as adults because CVID often goes unrecognized.
121
Q

Clinical Manifestations of X-linked agammaglobulinemia

A
  • usually symptoms appear after the natural loss of maternally transmitted immunoglobulins, which occurs at about 5 to 6 months of age
  • symptoms of recurrent pyogenic infections usually occur by that time
122
Q

Besides recurrent infection, patients with CVID are at increased risk for:

A
  • Autoimmune disease
  • granulomatous disease
  • malignancy
  • 20 to 22% of patients develop autoimmune diseases, notably autoimmune thrombocytopenic purpura and autoimmune hemolytic anemia.
  • Arthritis and hypothyroidism, frequently occur
  • More than 50% of patients with CVID develop pernicious anemia
123
Q

T-Cell Deficiencies lead to

A

Opportunistic infections

124
Q

Most primary T-cell immunodeficiencies are

A

genetic in origin

125
Q

Partial T-cell immunodeficiencies are commonly associated with

A

hyperimmune dysregulation, including autoimmune disorders, inflammatory diseases, and elevated IgG production.

126
Q

DiGeorge syndrome/thymic hypoplasia

A
  • is an example of a primary T-cell immunodeficiency.
  • mapped to chromosomes 10 and 22
  • rare, complex, multisystem genetic abnormality
  • affects multiple organ systems
127
Q

T-cell deficiency occurs when

A

The thymus gland fails to develop normally during embryogenesis.
-one of the few immunodeficiency disorders with symptoms that manifest almost immediately after birth

128
Q

Chronic mucocutaneous candidiasis

A
  • a rare T-cell disorder
  • thought to be autosomal recessive
  • affects both males and females
  • considered an autoimmune disorder involving the thymus and other endocrine glands
  • causes extensive morbidity resulting from endocrine dysfunction
129
Q

Clinical manifestations of DiGeorge syndrom

A

-infants born with it have hypoparathoridism with resultant hypocalcemia resistant to standard therapy, congenital heart disease, cleft palate and lip, dysmorphic facial features, and possibly renal abnormalities.

130
Q

Candidia albicans

A

is almost universal in patients with severe deficiencies in T-cell mediated immunity.

131
Q

The most frequent presenting sign in patients with DiGeorge syndrome is

A
  • hypocalcemia that is resistant to standard therapy.

- it usually occurs within the first 24 hours of life.

132
Q

Clinical manifestations of chronic mucocutaneous candidiasis

A

-may be the result of either chronic candida infection or idiopathic endocrinopathy
-persistent or recurrent candida infections of the skin, nails, and mucous membranes or by a variable combination of endocrine failure as well as
immunodeficiency
-patients may survive into the 2nd or 3rd decade of life
-problems may include hypocalcemia and tatany secondary to hypofunction of the parathyroid glands
-Hypofunction of the adrenal cortex (Addison’s disease) is the major cause of death in these patients; is may develop suddenly and without any history of previous symptoms.

133
Q

Patients with T-cell deficiency should receive

A
  • prophylaxis for PCP
  • management of hypocalcemia
  • correction of cardiac abnormalities
134
Q

Procedures used to permanently reconstitute T-cell immunity are:

A
  • Transplantation of fetal thymus
  • postnatal thymus
  • HLA-matched bone marrow transplant
135
Q

Combined B-cell and T-cell deficiencies

A
  • comprise a heterogenous group of disorders
  • all characterized by profound impairment in the development or function of the cellular, the humoral, or both parts of the immune system
  • a variety of inherited conditions fit the description
  • these conditions are typified by disruption of the normal communication system of B cells and T cells and impairment of the immune response, and they appear early in life.
136
Q

Ataxia-telangiectasia

A

autosomal recessive neurodegenerative disorder characterized by cereballa ataxia, telangiectasia (vascular lesions caused by dilated blood vessels), and immune deficiency.

137
Q

Severe combined immunodeficiency disease

A
  • is a disorder in which both B cells and T cells are missing
  • both cell0mediated and humoral functions are affected
  • SCID is marked by susceptibility to serious fungal, bacterial, and viral infections
  • one of the most common causes of primary immunodeficiencies.
138
Q

Wiskott-Aldrich syndrome (WAS)

A
  • a variation of SCID
  • inherited immunodeficiency caused by a variety of mutations in the gene encoding the WAS protein.
  • frequent infections, thrombocytopenia with small platelets, eczema, and increased risk of autoimmune disorders and malignancies.
  • prognosis is poor because most affected people develop overwhelming fatal infections.
139
Q

Deficiencies of the Complement system

A

Deficiencies in normal levels of C2 and C3 complement result in increased infecous diseases and immune-mediated disorders

140
Q

Hereditary angioneurotic edema

A

results from the deficiency of C1-esterase inhibitory, which opposes the release of inflammatory mediators

141
Q

S/S angioneurotic edema

A

recurrent attacks of edema formation in the subcutaneous tissue, gi tract, and upper airway

142
Q

Secondary immunodeficiencies

A
  • are more common than primary immunodeficiencies

- frequently occur as a result of underlying disease processes or the treatment of the disorders

143
Q

Common causes of secondary immunodeficiencies include:

A
  • chronic stress
  • burns
  • uremia
  • diabetes mellitus
  • certain autoimmune disorders
  • certain viruses
  • exposure to immunotoxic medications and chemicals
  • self-administration of recreational drugs and alcohol
144
Q

The most prevalent casue of immunodeficiency worldwide is

A

severe malnutrition

145
Q

The most common secondary disorder is

A

AIDS

146
Q

Nursing management for patients with immunodeficiencies

A
  • Assessment, patient education, selected interventions, supportive care
  • Assessment: for infection and timely initiation of treatment
  • Nursing care depends on the underlying cause of the immunodeficiency, the type and its severity
  • Monitor for s/s of infection
  • Many patients develop oral manifestations and need education about promoting good dental hygiene to diminish the oral discomfort and complications that frequently result in inadequate nutritional intake.
  • Pulse and r/r should be assessed for 1 full minute due to the possibility of subtle changes.
147
Q

Genetic testing r/t immunodeficiencies

A
  • testing is becoming available for many of the disorders
  • although this testing is rarely indicated in the initial workup for immunodeficiency
  • some deficiencies can be diagnosed by phenotype and functional assays.
  • genetic testing can establish or confirm a suspected diagnosis of some primary immune deficiencies
  • genetic testing is accomplished using whole blood samples and mouth swab samples.
148
Q

alpha-interferon

A

protein substance that the body produces in response to infection

149
Q

B-cell lymphoma

A

common malignancy in patients with HIV/AIDS

150
Q

Candidiasis

A

yeast infection of skin or mucous membrane

151
Q

CCR5

A

Along with the CD4+ receptor, this cell surface molecule is used by HIV to fuse with the host’s cell membranes

152
Q

cytomegalovirus

A

A species-specific herpes virus that may cause retinitis in people with AIDS

153
Q

EIA (enzyme immunoassay)

A

A blood test that can determine the presence of antibodies to HIV in the blood or saliva; also referred to ELISA (enzyme-linked immunosorbent assay). Positive results must be validated, usually with Western blot test.

154
Q

HIV-1

A

retrovirus isolated and recognized as the etiologic agent of AIDS

155
Q

HIV-2

A

retrovirus identified in 1986 in AIDS patients in West Africa.

156
Q

HIV encephalopathy

A

degenerative neurologic condition characterized by a group of clinical presentations including loss of coordination, mood swings, loss of inhibitions, and widespread cognitive dysfunctions; formerly referred to as AIDS dementia complex (ADC).

157
Q

human papillomavirus (HPV)

A

viruses that cause various warts, including plantar and genital warts; some strains of HPV can also cause cervical cancer

158
Q

Immune reconstitution inflammatory syndrome

A

a syndrome that results from rapid restoration of pathogen-specific immune responses to opportunistic infections; most often occurs after starting antiretroviral therapy

159
Q

Kaposi’s sarcoma

A

malignancy that involves the epithelial layer of blood and lymphatic vessels

160
Q

Latent reservoir

A

The integrated HIV provirus within the CD4+ T cell during the resting memory state; does not express viral proteins and is invisible to the immune system and antiviral medications.

161
Q

Macrophage

A

Large immune cell that devours invading pathogens and other intruders; can harbor large quantities of HIV without being killed, acting as a reservoir of the virus

162
Q

Monocyte

A

large white blood cell that ingests microbes or other cells and foreign particles. When a monocyte enters tissues, it develops into a macrophage.

163
Q

Mycobacterium avium complex

A

Opportunistic infection caused by mycobacterial organisms that commonly causes a respiratory illness but can also infect other body systems.

164
Q

Opportunistic infection

A

illness caused by various organisms, some of which usually do not cause disease in people with normal immune systems

165
Q

P24 antigen

A

blood test that measures viral core protein; accuracy of test is limited because the p24 antibody binds with the antigen and makes it undetectable

166
Q

Peripheral neuropathy

A

disorder characterized by sensory loss, pain, muscle weakness, and wasting of muscles in the hands or legs and feet

167
Q

Pneumocystis pneumonia or Pneumocystis jiroveci pneumonia (PCP)

A

common opportunistic lung infection caused by an organism, believed to be a fungus based on its structure

168
Q

Polymerase chain reaction

A

A sensitive laboratory technique that can detect and quantify HIV in a person’s blood or lymph nodes

169
Q

Primary infection

A

4- to 7-week period of rapid viral replication immediately following infection; also known as acute HIV infection

170
Q

Progressive multifocal leukoencephalopathy

A

Opportunistic infection that infects brain tissue and causes damage to the brain and spinal cord.

171
Q

Protease inhibitor

A

Medication that inhibits the function of protease, an enzyme needed for HIV replication

172
Q

Provirus

A

viral genetic material in the form of DNA that has been integrated into the host genome. When it is dormant in human cells, HIV is in a proviral form.

173
Q

Retrovirus

A

A virus that carries genetic material in RNA instead of DNA and contains reverse transcriptase

174
Q

Reverse Transcriptase

A

Enzyme that transforms single-stranded RNA into a double-stranded DNA

175
Q

Viral load test

A

Measures the quantity of HIV RNA in the blood

176
Q

Viral set point

A

amount of virus present in the blood after the initial burst of viremia and the immune response that follows.

177
Q

Wasting syndrome

A

Involuntary weight loss of 10% baseline body weight with chronic diarrhea or chronic weakness and documented fever

178
Q

Western blot assay

A

A blood test that identifies antibodies to HIV and is used to confirm the results of an EIA (ELISA) test

179
Q

Window period

A

Time from infection with HIV until seroconversion detected on HIV antibody test.

180
Q

When did the FDA approve the first antiretroviral agent?

A
  • 1987
  • Just 6 years after the 1st case of AIDS was reported
  • Currently more than 25 antiretroviral medications are available in the US.
181
Q

When did the HIV, EIA (formerly ELISA) test become available?

A

-1984

182
Q

How is HIV-1 transmitted?

A
  • body fluids that contain free virions and infected CD4+ T cells.
  • Blood, seminal fluid, amniotic fluid, breat milk
  • Inflammation and breaks in the skin or mucosa result in the increased probability that an exposure to HIV will lead to infection
183
Q

Mother-to-child transmission of HIV-1 may occur:

A
  • In utero
  • At the time of delivery
  • through breast-feeding
  • *most perinatal infections are thought to occur after exposure during delivery.
  • *HIV is not transmitted through casual contact
184
Q

Preventive Education

A

-Evidence-based programs r/t safer sex practices

185
Q

What is the only effective method to decrease the risk of sexual transmission of HIV infection?

A

Other than abstinence it is consistent and correct use of condoms.

186
Q

When male condoms are used consistently during vaginal or anal intercourse, their effectiveness can be as high as:

A

95%

187
Q

Non-latex condoms made of natural materials such as lambskin are available for people with latex allergy but will not do what?

A

Protect against HIV infection.

188
Q

The polyurethane female condom, which is an effective contraceptive, provides what?

A
  • A physical barrier that also prevents exposure to genital secretions containing HIV such as semen and vaginal fluid.
  • The only barrier method that can be controlled by the woman.
189
Q

Microbicides are:

A

Chemical products such as gels, creams, films, or suppositories that are inserted into the vagina or rectum before sexual intercourse to prevent HIV transmission.

190
Q

Circumcision and HIV prevention

A

-recognized as an effective strategy to reduce the risk of HIV acquisition in men because the presence of the foreskin, which harbors HIV target cells, might facilitate survival and entry of the virus.

191
Q

Harm Reduction Model

A
  • recognizes that total abstinence from addictive drugs might not be a realistic short-term goal.
  • recommends working with drug users to assist them to increase their healthy behaviors
  • clean/sterile needles at no cost
  • extensive research proves that needle exchange drug programs DO NOT increase drug use
192
Q

HIV related reproductive education

A
  • Because HIV infection in women often occurs during the childbearing years, family planning issues need to be addressed
  • Artificial insemination
  • HIV + mothers should not breast-feed as HIV is transmitted through breast milk
  • Avoid estrogen based oral contraceptives
  • Avoid IUD because string can transmit the virus.
193
Q

To avoid transmission to health care providers, what does the CDC recommend?

A

Following standard precautions with every patient, every time.
Standard precautions: hand hygiene, PPE, soiled patient care equipment, environmental control, textiles and laundry, patient resuscitation, patient placement, respiratory hygiene/cough etiquette

194
Q

Viruses are

A

Intracellular parasites

195
Q

HIV belongs to a group of viruses known as:

A

Retroviruses

196
Q

Retroviruses

A

Carry their genetic material in the form of ribonucleic acid (RNA) rather than deoxyribonucleic acid (DNA).

197
Q

The structure of HIV is:

A

a viral core containing the viral RNA, surrounded by an envelope consisting of protruding glycoproteins.

198
Q

All viruses target specific cells. HIV targets cells with:

A

CD4 receptors, which are expressed on the surface of T lymphocytes, monocytes, dendritic cells, and brain microglia.

199
Q

Mature T cells

A
  • T Lymphocytes

- Composed of 2 major subpopulations that are defined by cell surface receptors of CD4 or CD8

200
Q

T cell anatomy

A
  • Approximately 2/3 of peripheral blood T cells are CD4+
  • Approximately 1/3 of peripheral blood T cells are CD8+
  • Most people have about 700 to 1000 CD4+ cells/mm3
  • Levels as low as 500 cells/mm3 can be considered WNL
201
Q

How does HIV fuse with the T cell?

A
  • most varieties of HIV-1 use the chemokine receptor CCR5 (R5 virus) for entry to T cells in addition to the CD4+ receptor
  • The glycoproteins of HIV attach to both the CD4+ and the CCR5 binding sites and bind to the CD4+ cell membrane, resulting in fusion of HIV with the T cell.
202
Q

HIV life cycle

A
  • is complex and follows these steps:
  • Attachment
  • Uncoating
  • DNA synthesis
  • Integration
  • Transcription
  • Translation
  • Clevage
  • Budding
203
Q

The stage of HIV disease is based on:

A
  • Clinical history
  • Physical examination
  • Laboratory evidence of immune dysfunction
  • Signs and symptoms
  • Infections and malignancies
204
Q

Primary HIV infection

A
  • The period from infection with HIV to the development of HIV-specific antibodies
  • Characterized by high levels of viral replication, widespread dissemination of HIV throughout the body, and destruction of CD4+ T -cell counts
205
Q

Window period

A

an HIV-positive person tests negative on the HIV antibody blood test, although he or she is infected and highly infectious, because his or her viral load is very high.
-After 2 to 3 weeks, antibodies to the glycoproteins of the HIV envelope can be detected in the sera of HIV-infected people

206
Q

Viral set point

A
  • Remaining amount of HIV in the body after the initial immune response
  • The final level of the viral set point is inversely correlated with disease prognosis; that is, the higher the viral set point, the poorer the prgnosis
207
Q

CDC Category A

A
  • the acute symptomatic and early infection phases
  • during this phase the virus is widely disseminated in lymphoid tissue, and a latent reservoir within resting memory CD4+ T cells is created
208
Q

On average, HIV-related complications develop

A

8 - 10 years after diagnosis

209
Q

HIV testing guidelines

A
  • HIV screening is recommended for all patients 18 to 64 years of age
  • High risk should be screened annually
  • General consent for medical care is sufficient
  • Prevention counseling should not be required
210
Q

HIV antibody testing

A
  • EIA (enzyme immunoassay): formerly known as ELISA, identifies antibodies directed specifically against HIV
  • Western Blot: used to confirm seropositivity when the EIA result is positive.
211
Q

Seropositive

A

blood containing antibodies for HIV

212
Q

OraSure test

A
  • uses saliva to perform an EIA antibody test

- becoming the standard method of testing in settings where a delay would seriously affect treatment (ER/OB)

213
Q

HIV Infection Treatment

A
  • protocols on how and when to treat change relatively often
  • antiretroviral medications should be offered to people with a T-cell count of less than 350 cells/mm3 or plasma HIV RNA levels exceeding 100,000 copies/mL.
214
Q

Antiretroviral drug classes

A
  • Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)
  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
  • Protease inhibitors (PIs)
215
Q

To achieve sustained viral suppression, patients must take:

A

more than one antiretroviral medication

216
Q

Results of HIV therapy are evaluated with

A

Viral load tests

217
Q

An HIV + patient may test positive when their viral load falls below what level?

A

50 RNA copies/mL

218
Q

HIV drug resistance

A
  • can be broadly defined as the ability of pathogens to withstand the effects of medications that are intended to be toxic to them
  • 2 major components of antiretroviral drug resistance:
    1. transmission of drug-resistant HIV at the time of initial infection
    1. selective drug resistance in patients who are receiving non-suppressive regimens.
219
Q

Factors associated with the development of drug resistance include:

A
  • monotherapy
  • difficulty with adherence to complex and toxic regimens
  • initiation of therapy late in the course of HIV/AIDS
220
Q

Immune reconstitution inflammatory syndrome (IRIS)

A

-results from rapid restoration of pathogen-specific immune responses to opportunistic infections that cause either the deterioration of a treated infection or new presentation of a subclinical infection.

221
Q

The clinical manifestations of HIV/AIDS are

A

Widespread and may involve virtually any organ system.

222
Q

Respiratory Manifestations of HIV

A
  • shortness of breath
  • dyspnea (labored breathing)
  • cough
  • chest pain
  • fever
  • *all these symptoms are associated with various opportunistic infections, such as those caused by P. jiroveci, Mycobacterium avium-intracellular, CMV, and Legionella species.
223
Q

Pneumocystis pneumonia (HIV)

A
  • PCP
  • the most common infection in people with AIDS
  • caused by P. jiroveci
  • w/o prophylactic therapy, 80% of all people with HIV will develop PCP.
  • clinical presentation of PCP in HIV infection is generally less acute than in people who are immunosuppressed as a result of other conditions.
224
Q

Mycobacterium avium complex (MAC) - in HIV+ patients

A
  • a common opportunistic infection in people with AIDS
  • MAC comprises a group of acid-fast bacilli (mycobacteria) that includes M. avium, M. intracellular, and M. scrofulaceum.
  • It usually causes respiratory infection but is also commonly found in the GI tract, lymph nodes, and bone marrow.
  • associated with rising mortality rates
  • T-cell counts lower than 100 cells/mm3 have widespread disease at diagnosis and are debilitated.
225
Q

Tuberculosis (HIV)

A
  • in HIV positive people have a risk of latent TB of 10%, annually
  • TB can develop in the lungs as well as in extrapulmonary sites such as the CNS, bone, pericardium, stomach, peritoneum, and scrotum.
  • CD4 T-cell count influences both the frequency and clinical picture of active TB disease.
226
Q

GI Manifestations (HIV)

A
  • manifestations w/ AIDS include loss of appetite, nausea, vomiting, oral and esophageal candidiasis, and chronic diarrhea.
  • diarrhea is a problem in 50-90% of all AIDS patients
  • GI symptoms may be r/t the direct effect of HIV on the cells lining the intestines.
227
Q

Wasting syndrome

A
  • part of the category C case definition for AIDS.
  • involuntary weight loss exceeding 10% of baseline body weight
  • Protein-energy malnutrition; multifactorial
228
Q

Oncologic Manifestations w/ AIDS

A
  • Kaposi’s sarcoma
  • Lymphoma
  • Non-Hodgkin lymphoma
  • Invasive cervical cancer
229
Q

Kaposi’s Sarcoma

A
  • KS
  • the most common HIV related malignancy
  • a disease that involves the endothelial layer of blood and lymphatic vessels
230
Q

B-Cell Lymphomas (HIV/AIDS)

A
  • the 2nd most common malignancy occurring in people with AIDS
  • non-Hodgkin lymphoma (younger patients)
  • develop outside the lymph nodes, most commonly in the brain, bone marrow, and GI tract.
  • aggressive growth, resistance to treatment
231
Q

Neurologic Manifestations (HIV/AIDS)

A
  • HIV dementia
  • HIV-associated neurocognitive disorders
  • motor dysfunction and behavioral change
232
Q

HIV encephalopathy

A

-formerly called AIDS dementia complex

233
Q

Cryptococcus neoformans

A
  • fungal infection
  • common opportunistic infection among AIDS patients
  • causes neurologic disease
  • s/s: fever, headache, malaise, stiff neck, N/V, mental status changes, and seizures.
  • Diagnosis is made by CSF analysis
234
Q

Care of the patient with HIV encephalitis

A
  • Disturbed thought process
  • Disturbed sensory perception
  • Risk for injury
  • Self-care deficits
235
Q

Progressive Multifocal Leukoencephalopathy

A
  • PML
  • a demyelinating CNS disorder
  • affects the oligodendroglia
  • Clinical manifestations: mental confusion, blindness, aphasia, muscle weakness, paresis, and death
236
Q

Cytomegalovirus retinitis

A

-retinitis caused by CMV is a leading cause of blindness in patients with AIDS

237
Q

Antidiarrheal therapy

A

-therapy with octreotide acetate (Sandostatin), a synthetic analogue of somatostatin, has been shown to be effective

238
Q

Chemotherapy (Kaposi’s sarcoma/ Lymphoma)

A
  • management of KS is usually difficult because of the variability of symptoms and the organ systems involved.
  • KS is rarely life-threatening except when there is pulmonary or gi involvement.
  • Treatment goals for KS: reduce s/s by decreasing the size of the skin lesions, reduce discomfort associated with edema and ulcerations, and to control s/s associated with mucosal or visceral involvement.
  • Successful tx of AIDS-related lymphomas has been limited b/c of the rapid progression of these malignancies.
  • Initial response then no response to chemo and radiation
239
Q

Diet for patients with diarrhea

A

-low in fat, lactose, insoluble fiber, and caffeine and high in soluble fiber

240
Q

Allergen

A

substance that causes manifestations of allergy

241
Q

Allergy

A

inappropriate and often harmful immune system response to substances that are normally harmless

242
Q

Anaphylaxis

A

Clinical response to an immediate immunologic reaction between a specific antigen and antibody

243
Q

Angioneurotic edema

A

condition characterized by urticarial and diffuse swelling of the deeper layers of the skin

244
Q

Antibody

A

protein substance developed by the body in response to and interacting with a specific antigen

245
Q

Antigen

A

substance that induces the production of antibodies

246
Q

Antihistamine

A

medication that opposes the action of histamine

247
Q

Atopic dermatitis

A

type I hypersensitivity involving inflammation of the skin evidenced by itching, redness, and a variety of skin lesions

248
Q

Atopy

A

term often used to describe immunoglobulin E-mediated diseases (ie, atopic dermatitis, asthma, and allergic rhinitis) with a genetic component

249
Q

B lymphocytes

A

cells that are important in producing circulating antibodies

250
Q

bradykinin

A

a substance that stimulates nerve fibers and causes pain

251
Q

eosinophil

A

granular leukocyte

252
Q

Erythema

A

diffuse redness of the skin

253
Q

hapten

A

incomplete antigen

254
Q

histamine

A

substance in the body that causes increased gastric secretion, dilation of capillaries, and constriction of the bronchial smooth muscle

255
Q

hypersensitivity

A

abnormal heightened reaction to a stimulus of any kind

256
Q

immunoglobulins

A

a family of closely related proteins capable of acting as antibodies

257
Q

leuokotrienes

A

a group of chemical mediators that initiate the inflammatory response

258
Q

mast cells

A

connective tissue cells that contain heparin and histamine in their granules

259
Q

prostaglandins

A

unsaturated fatty acids that have a wide assortment of biologic activity

260
Q

rhinitis

A

inflammation of the nasal mucosa

261
Q

Serotonin

A

chemical mediator that acts as a potent vasoconstrictor and bronchoconstrictor

262
Q

T lymphocytes

A

cells that can cause graft rejection, kill foreign cells, or suppress production of antibodies

263
Q

Urticaria

A

hives

264
Q

Epithelial cells

A
  • coat the skin
  • make up the lining of the respiratory, GI, & GU tracts
  • provide first line defense against microbial invaders
  • the structure and continuity of these surfaces and their resistance to penetration are initial deterrents to invaders
265
Q

Antibodies react with antigens in a variety of ways:

A
  1. by coating the antigens’ surfaces if they are particular substances
  2. by neutralizing the antigens if they are toxins
  3. by precipitating the antigens out of solution if they are dissolved
    - The antibodies prepare the antigens so that the phagocytic cells of the blood and the tissues can dispose of them.
266
Q

Allergic reaction

A

-a manifestation of tissue injury resulting from interaction between an antigen and an antibody.

267
Q

Antigens are divided into two groups:

A
  • complete protein antigens &

- low-molecular-weight substances (haptens)

268
Q

Histamine effects are greatest within:

A

about 15 minutes after antigen contact.

269
Q

Histamine action results from stimulation of:

A
  • histamine-1 (H1) receptors: found predominantly on bronchiolar and vascular smooth muscle cells;
  • histamine-2 (H2) receptors: found on gastric parietal cells
270
Q

Antihistamine medication for H1 receptors

A

diphenhydramine (Benadryl)

271
Q

Antihistamine medication for H2 receptors

A

cimetidine (Tagamet)
ranitidine (Zantac)
**these target H2 receptors to inhibit gastric secretions in peptic ulcer disease

272
Q

Eosinophil Chemotactic Factor of Anaphylaxis

A
  • affects movement of eosinophils (granular leukocytes) to the site of allergens
  • is performed in the mast cells
  • is released from disrupted mast cells
273
Q

Platelet-Activating Factor

A
  • responsible for initiating platelet aggregation and leukocyte infiltration at sites of immediate hypersensitivity reactions
  • causes bronchoconstriction and increased vascular permeability
274
Q

Prostaglandins

A
  • produce smooth muscle contractions
  • produce vasodilation
  • produce increased capillary permeability
  • *the fever and pain that occur with inflammation in allergic responses are caused in part by the prostaglandins.
275
Q

Leukotrienes

A
  • chemical mediators that initiate the inflammatory response
  • cause smooth muscle contraction
  • cause bronchial constriction
  • cause mucus secretion in the airways
  • cause the typical wheal-and-flare reactions of the skin
  • compared to histamines, leukotrienes are 100 to 1000 times more potent in causing bronchospasm.
276
Q

Bradykinin

A
  • a substance that has the ability to cause increased vascular permeability, vasodilation, hypotension, and contraction of many types of smooth muscle, such as the bronchi.
  • increased permeability of the capillaries results in edema
  • it stimulates nerve cell fibers and produces pain
277
Q

Serotonin

A

acts as a potent vasoconstrictor and causes contraction of bronchial smooth muscle.

278
Q

Most allergic reactions are what type of hypersensitivity reactions?

A

type I or type IV

279
Q

Anaphylactic Hypersensitivity

A
  • Type I
  • an unanticipated severe allergic reaction that is often explosive in onset
  • edema in many tissues, including the larynx, and is often accompanied y hypotension, bronchospasm, and cardiovascular collapse in severe cases
  • an immediate reaction beginning within minutes of exposure to an antigen
  • primary chemical mediators are responsible for the symptoms of a type I reaction because of their effects on the skin, lungs, and GI tract.
  • a delayed reaction may occur for up to 24 hours
  • this reaction may include both local and systemic anaphylaxis
280
Q

Cytotoxic Hypersensitivity

A
  • Type II
  • occurs when the system mistakenly identifies a normal constituent of the body as foreign
  • may be the result of a cross-reacting antibody, possibly leading to cell and tissue damage
  • associated with several disorders; myasthenia gravis, Goodpasture syndrome
  • a type II reaction resulting in RBC destruction is associated with drug-induced immune hemolytic anemia, Rh-hemolytic disease of the newborn, and incompatibility reactions in blood transfusions.
281
Q

Immune complex hypersensitivity

A
  • Type III
  • involves immune complexes that are formed when antigens bind to antibodies
  • these complexes are cleared from the circulation by phagocytic action
  • if these type III complexes are deposited in tissues or vascular endothelium, two factors contribute to injury: the increased amount of circulating complexes and the presence of vasoactive amines
  • the result is an increase in vascular permeability and tissue injury
  • joints and kidneys are particularly susceptible to this type of injury
  • type III is associated with systemic lupus erythematosus, rheumatoid arthritis, certain types of nephritis, and some types of bacterial endocarditis
282
Q

Delayed-type hypersensitivity

A
  • Type IV
  • also known as cellular hypersensitivity
  • occurs 24 to 72 hours after exposure to an allergen
  • mediated by sensitized T cells and macrophages rather than antibodies
  • an example is contact dermatitis resulting from exposure to allergens such as cosmetics, adhesive tape, topical agents, medication additives, and plant toxins
  • Symptoms include: itching, erythema, and raised lesions
283
Q

Substances that most commonly cause anaphylactic reaction:

A

Food, medication, insect stings, and latex:

  • Food: peanuts, tree nuts (walnuts, pecans, cashews, almonds), shellfish, fish, milk, eggs, soy, wheat
  • Medication: antibiotics, especially PCN and Sulfa, allopurinol, radiocontrast agents, anesthetic agents, vaccines, hormones, aspirin, NSAIDs
  • Insect stings: bees, wasps, hornets, yellow jackets, ants, including fire ants
  • PCN is the most common cause of anaphylaxis and accounts for about 75% of fatal anaphylactic reactions in the US each year.*
284
Q

Medical management following injection of epinephrine

A
  • transport to the local ER for observation and monitoring
  • rebound reaction can happen 4 to 10 hours after the initial allergic reaction
  • patients with more severe reactions are monitored closely for 12 to 14 hours in a facility that can provide emergency care
285
Q

Seasonal allergens

A

Early spring - tree pollen
Early summer - rose pollen, grass pollen
early fall - weed pollen (ragweed)

286
Q

Avoidance therapy

A

-every attempt is made to remove the allergens that act as precipitating factors

287
Q

Antihistamine medications:

A
  • now classified as H1 receptor antagonists (or H1-blockers),
  • used in the management of mild allergic disorders
  • the major class of medications prescribed for the symptomatic relief of allergic rhinitis.
288
Q

Adrenergic agents

A
  • vasoconstrictors of mucosal vessels
  • used topically in addition to the oral route
  • topical (drops/sprays) cause fewer side effects than oral administration
  • tops/sprays limited to only a few days to avoid rebound congestion
289
Q

Mast Cell Stabilizers

A
  • intranasal cromolyn sodium: spray that acts by stabilizing the mast cell membrane
  • inhibits macrophages, eosinophils, monocytes, and platelets involved in the immune response
  • interrupts the physiologic response to nasal antigens
  • is used prophylactically
290
Q

Corticosteriods

A
  • indicated in more severe cases of allergic and perennial rhinitis that cannot be controlled by more conventional medications
  • Examples are: beclomethasone, budesonide, dexamethasone, flunisolide, fluticasone, and triamcinolone.
  • administered by metered-spray devices
  • full benefit may take up to 2 weeks.
291
Q

Leukotriene Modifiers

A
  • zileuton, zafirlukast, montelukast
  • block the synthesis or action of leukotrienes and prevent the s/s associated with asthma
  • for long-term use
  • take medication daily
292
Q

Immunotherapy

A
  • allergen desensitization
  • primarily used to treat IgE-mediated diseases by injections of allergen extracts
  • also called allergy vaccine therapy
  • goal is to reduce the circulating IgE and increase the level of blocking antibody IgG, and reducing mediator cell sensitivity.
  • therapy takes 3 to 5 years
  • monitor patient in clinic for 30 minutes after each injection
293
Q

Latex allergy cross contaminations

A

Cross-reactions have been reported in people who are allergic to certain food products, such as kiwis, bananas, pineapples, mangos, passion fruit, avocados, and chestnuts.

Med Surg II (4 decks)

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