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ANAPHY LECTURE > Body Defense > Flashcards

Body Defense Flashcards

1
Q

Two types of mechanisms defend the body against these tiny but mighty enemies:

A

innate and adaptive defense mechanisms

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2
Q

is a functional system rather than an organ system in an anatomical sense.

A

the immune system

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3
Q

The most important of the
immune cells are

A

lymphocytes, dendritic cells,
and macrophages.

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4
Q

play an important role in both innate and adaptive mechanisms.

A

Macrophages

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5
Q

also called the nonspecific defense system, responds immediately to protect the body from all foreign substances, whatever they are

A

innate defense system

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6
Q

Innate (nonspecific) defense mechanisms- First line of defense

A
  • Skin
  • Mucous membranes
  • Secretions of skin
    and mucous
    membranes
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7
Q

Innate (nonspecific) defense mechanisms- Second line of defense

A
  • Phagocytic cells
  • Natural killer cells
  • Antimicrobial proteins
  • The inflammatory
    response
  • Fever
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8
Q

Adaptive (specific) defense
mechanisms- Third line of defense

A
  • Lymphocytes
  • Antibodies
  • Macrophages and other
    antigen-presenting cells
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9
Q

reduce the workload of the adaptive defense mechanisms by generally preventing the entry and spread of microorganisms throughout the body.

A

innate mechanisms

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10
Q

or specific defense system, fights invaders that get past the innate defenses by mounting an attack against one or more particular foreign substances.

A

adaptive defense system

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11
Q

The resulting highly specific resistance to disease is called

A

immunity

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12
Q

Another important feature of the adaptive response is that it

A

“remembers” which invaders it has fought

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13
Q

refers to the mechanical barriers that cover body surfaces and to the cells and chemicals that act on the initial battlefronts to protect the body from invading pathogens (harmful microorganisms)

A

innate, or nonspecific, body defense

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14
Q

The body’s first line of defense against the invasion of disease-causing microorganisms includes the

A

skin and mucous membranes

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15
Q

Forms mechanical barrier that prevents entry of pathogens and other harmful substances into body.

A

Intact skin (epidermis)

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16
Q

Skin secretions make epidermal surface acidic, which inhibits
bacterial growth; sebum also contains bacteria-killing chemicals.

A

Acid mantle

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17
Q

Provides resistance against acids, alkalis, and bacterial enzymes.

A

Keratin

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18
Q

Form mechanical barrier that prevents entry of pathogens

A

Intact mucous membranes

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19
Q

Traps microorganisms in respiratory and digestive tracts.

A

Mucus

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20
Q

Filter and trap microorganisms and other airborne particles in nasal
passages.

A

Nasal hairs

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21
Q

Propel debris-laden mucus away from lower respiratory passages.

A

Cilia

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22
Q

Contains concentrated hydrochloric acid and protein-digesting
enzymes that destroy pathogens in stomach.

A

Gastric juice

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23
Q

Inhibits growth of bacteria and fungi in female reproductive tract.

A

Acid mantle of vagina

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24
Q

Continuously lubricate and cleanse eyes (tears) and oral cavity
(saliva); contain lysozyme, an enzyme that destroys microorganisms.

A

Lacrimal secretion (tears); saliva

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25
Q

Engulf and destroy pathogens that breach surface membrane
barriers; macrophages also contribute to immune response.

A

Phagocytes

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26
Q

Promote cell lysis by direct cell attack against virus-infected or
cancerous body cells; do not depend on specific antigen recognition.

A

Natural killer cells

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27
Q

Prevents spread of injurious agents to adjacent tissues, disposes of
pathogens and dead tissue cells, and promotes tissue repair; releases
chemical mediators that attract phagocytes (and immune cells) to
the area.

A

Inflammatory response

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28
Q

Group of plasma proteins that lyses microorganisms, enhances
phagocytosis by opsonization, and intensifies inflammatory response.

A

Complement

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29
Q

Proteins released by virus-infected cells that protect uninfected tissue
cells from viral takeover; mobilize immune system.

A

Interferons

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30
Q

Normally acid pH inhibits bacterial growth; urine cleanses the lower
urinary tract as it flushes from the body.

A

Fluids with acid pH

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31
Q

Systemic response triggered by pyrogens; high body temperature
inhibits multiplication of bacteria and enhances body repair
processes.

A

fever

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32
Q

The acidic pH of skin secretions

A

acid mantle

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33
Q

pH level of urine

A

4.5 to 6

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34
Q

traps many microorganisms that enter digestive and respiratory passageways.

A

Sticky mucus

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35
Q

secretes gastric juice containing hydrochloric acid and protein-digesting enzymes that both kill pathogens.

A

stomach mucosa

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36
Q

stomach mucosa secretes containing hydrochloric acid and protein-digesting enzymes that both kill pathogens.

A

gastric juice

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37
Q

Saliva and lacrimal secretions (tears) contain an enzyme that destroys bacteria.

A

lysozyme

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38
Q

preventing particles from entering the lungs, where the warm, moist environment provides ideal conditions for bacterial growth. (think “sticky trap”)

A

The cilia sweep dust- and bacteria-laden mucus

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39
Q

For its second line of defense, defenses rely on the destructive powers of cells called

A

phagocytes and natural killer cells

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40
Q

roam the body in blood and lymph. They are a unique group of aggressive lymphocytes.

A

Natural killer (NK) cells

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41
Q

cells can act spontaneously against any such target by recognizing certain sugars on the “intruder’s” surface as well as its lack of certain “self” cell surface molecules

A

Natural killer (NK) cells

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42
Q

not phagocytic. They attack the target cell’s membrane and release lytic chemicals
called perforin and granzymes. also release powerful inflammatory chemicals.

A

NK cells

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43
Q

NK cells attack the target cell’s membrane and release lytic chemicals called

A

perforin and granzymes

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44
Q

is a nonspecific response that is triggered whenever body tissues are injured

A

inflammatory response

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45
Q

The four most common indicators, or cardinal signs, of acute inflammation are

A
  1. redness
  2. heat (inflamm = set on fire)
  3. pain
  4. swelling (edema)
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46
Q

The inflammatory process begins with a

A

chemical “alarm”

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47
Q

When cells are damaged, they release inflammatory chemicals, including

A

histamine and kinins

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48
Q

3 phenomenon when cells are damaged

A

(1) cause blood vessels in the area to dilate
(2) make capillaries leaky
(3) attract phagocytes and
white blood cells to the area.

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49
Q

the 3rd phenomenon when cells are damaged called

A

positive chemotaxis

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50
Q

the cells are moving toward a high concentration of signaling molecules

A

positive chemotaxis (third phenomenon)

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51
Q

Increased permeability of the capillaries allows fluid to leak from the blood into the tissue spaces, causing

A

local edema (swelling)

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52
Q

Some authorities consider limitation of joint movement to be the

A

fifth cardinal sign of inflammation.

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53
Q

prevents the spread of damaging agents to nearby tissues, disposes of cell debris and pathogens, and sets the stage for repair

A

inflammatory response

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54
Q

inflammatory process

A
  1. Neutrophils enter blood from bone marrow, following the “scent.”
    and roll along the vessel wall
  2. Diapedesis- flatten out and squeeze
    through the capillary walls, chemical signal is the strongest
  3. Positive chemotaxis, the gradient of inflammatory chemicals. the neutrophils gather at the site of tissue injury
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55
Q

At the point where the chemical signal is the strongest, they flatten out and squeeze through the capillary walls, a process

A

Diapedesis

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56
Q

responding to a gradient of diffusing inflammatory chemicals

A

Neutrophils

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57
Q

follow neutrophils into the inflamed area, fairly poor phagocytes and after entering the tissues they become macrophages with insatiable appetites

A

monocytes

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58
Q

continue to wage the battle, replacing the short-lived neutrophils at the site of damage.

A

macrophages

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59
Q

are the central actors in the final disposal of cell debris as the inflammation subsides.

A

macrophages

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60
Q

leaked into the area from the blood, are activated and begin to wall off the damaged area with fibrin to prevent the spread of harmful agents to neighboring tissues

A

Clotting proteins

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61
Q

also forms scaffolding for permanent repair

A

fibrin mesh

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62
Q

is a mixture of dead or dying neutrophils, broken-down tissue cells, and living and dead pathogens.

A

Pus

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63
Q

If the inflammatory mechanism fails to fully clear the area of debris, the sac of pus may become walled off, forming an

A

abscess

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64
Q

Pathogens that make it through the mechanical barriers are confronted by

A

phagocytes

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65
Q

A phagocyte, engulfs a foreign particle by the process of phagocytosis, such as a

A

macrophage or neutrophil

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66
Q

enhance the innate defenses either by attacking microorganisms directly or by hindering their ability to reproduce

A

antimicrobial proteins

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67
Q

it refers to a group of at least 20 plasma proteins that circulate in the blood in an inactive state, inactive clotting proteins

A

complement

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68
Q

occurs when complement proteins bind to certain sugars or proteins (such as antibodies) on the foreign cell’s surface

A

complement fixation

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69
Q

result of complement fixation:

A
  1. the formation of membrane attack complexes (MAC) that produce holes, or pores, in the foreign cell’s surface.
  2. These pores allow water to rush into the cell
  3. causing it to burst, or lyse.
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70
Q

produce holes, or pores, in the foreign cell’s surface.

A

membrane attack complexes (MAC)

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71
Q

Some of the molecules released during the activation process are

A

vasodilators, and some are chemotaxis chemicals

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72
Q

attract neutrophils and macrophages into
the region

A

chemotaxis chemicals

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73
Q

this effect cause the cell membranes of the foreign cells to become sticky so they are easier to phagocytize

A

opsonization

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74
Q

is a nonspecific defensive mechanism that “complements,” or enhances, the effectiveness of both innate and adaptive defenses

A

Complement

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75
Q

Complement proteins must be activated in a particular sequence, which insures that complement is not accidentally activated, is called

A

cascade

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76
Q

acellular particles—essentially nucleic acids surrounded by a protein coat—that lack the cellular machinery required to generate ATP or make proteins.

A

viruses

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77
Q

does “dirty work” in the body by taking over target cells

A

viruses

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78
Q

viruses uses to reproduce themselves

A

cellular machinery and nutrients

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79
Q

virus-infected cells defend cells that have not yet been infected by secreting small proteins called

A

interferons

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80
Q

diffuse to nearby cells and bind to their
membrane receptors

A

interferon molecules

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81
Q

abnormally high body temperature, is a systemic response to invading microorganisms.

A

Fever

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82
Q

Body temperature is regulated by the body’s “thermostat.”

A

hypothalamus

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83
Q

a group of chemically diverse substances that cause fever and shock in severe cases

A

pyrogens

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84
Q

stalks and eliminates with nearly equal precision almost any type of pathogen that intrudes into the body.

A

specific defense system

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85
Q

response to a threat involves tremendously increased internal nonspecific defenses

A

immune response

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86
Q

the adaptive, or specific, defense mechanism is a functional system that recognizes foreign molecules called antigens and acts to inactivate or destroy them.

A

antigens

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87
Q

animals surviving a serious bacterial infection have “factors” in their blood that protect them from future attacks by the same pathogen

A

antibodies

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88
Q

These landmark experiments revealed three important aspects of adaptive defense:

A
  1. It is antigen specific
  2. It is systemic
  3. It has “memory”
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89
Q

important aspects of adaptive defense, immunity is not restricted to the initial infection site.

A

It is systemic

90
Q

important aspects of adaptive defense, it recognizes and actsagainst particular pathogens or foreign substances.

A

It is antigen specific

91
Q

important aspects of adaptive defense, it recognizes and mounts even stronger attacks on previously encountered pathogens.

A

It has “memory”

92
Q

also called antibody-mediated immunity, is provided by antibodies (immune proteins) present in the body’s “humors,” or fluids

A

Humoral immunity

93
Q

When lymphocytes themselves defend the body, the immunity is called

A

cellular immunity or cell-mediated immunity

94
Q

act against such targets either directly, by lysing the foreign cells, or indirectly, by releasing chemicals that enhance the inflammatory response or activate other immune cells

A

lymphocytes

95
Q

is any substance capable of provoking an immune response

A

antigen

96
Q

are large, complex molecules that are not normally present in our bodies, non-self.

A

Foreign antigen

97
Q

As a rule, small molecules are not antigenic, but when they link up with our own proteins,

A

hapten or incomplete antigen

98
Q

The crucial cells of the adaptive system are

A

lymphocytes and antigen-presenting cells (APCs)

99
Q

Lymphocytes exist in twoother major “flavors.”

A

B lymphocytes or B cells and T lymphocytes or T cells

100
Q

produce antibodies and oversee humoral
immunity

A

B lymphocytes or B cells

101
Q

constitute the cell-mediated arm of the adaptive defenses and do not make antibodies

A

T lymphocytes, or T cells

102
Q

can recognize and eliminate specific virus-infected or tumor cells

A

T lymphocytes, or T cells

103
Q

can target specific extracellular antigens

A

B lymphocytes, or B cells

104
Q

do not respond to specific antigens but instead play an essential role in activating the lymphocytes that do

A

APCs

105
Q

immature lymphocytes, released from the marrow are essentially identical

A

naive

106
Q

migrate (in blood) to the thymus and develop immunocompetence there

A

T cells

107
Q

develop immunocompetence in red bone marrow

A

B cells

108
Q

sites of development of immunocompetence as B or T cells

A

Primary lymphoid organs

109
Q

site of lymphocyte origin

A

Red bone marrow

110
Q

sites of antigen encounter, and activation to become effector and memory B or T cells

A

Secondary lymphoid organs

111
Q

arise from lymphocytes that migrate to the thymus

A

t cells

112
Q

development of self-tolerance for the body’s own cells is an essential part of a

A

lymphocyte’s “education.”

113
Q

B cells develop immunocompetence in

A

bone marrow

114
Q

capable of responding to a specific antigen by binding to it with antigen specific receptors that appear on the lymphocyte’s surface

A

immunocompetent

115
Q

There they undergo a maturation process lasting 2 to 3 days, directed by thymic hormones

A

T cell in Thymus

116
Q

acting against body
cells

A

self-antigens

117
Q

Thus, it is our genes, not antigens, that determine what foreign substances our immune system will be able to recognize and resist

A

TRUE

118
Q

in immunity is to engulf antigens and then present fragments of them, like signal flags, on their own surfaces, where they can be recognized by T cells

A

antigen-presenting cells
(APCs)

119
Q

present antigens to the cells that will actually deal with the antigens

A

antigen-presenting cells
(APCs)

120
Q

The major types of cells acting as APCs are

A

dendritic cells, macrophages, and B lymphocytes.

121
Q

also called Langerhans cells, are present in connective tissues and in the epidermis

A

Dendritic cells

122
Q

are widely distributed throughout the lymphoid organs and connective tissues, where they act as phagocytes in the innate defense system

A

Macrophages

123
Q

true “killers” that are insatiable phagocytes and secrete bactericidal (bacteria killing) chemicals

A

activated macrophages

124
Q

are the most effective antigen presenters
known—it’s their only job. Key link between innate and adaptive immunity.

A

dendritic cells

125
Q

In this process, the lymphocyte begins to grow and then multiplies rapidly to form an army of cells exactly like itself and bearing the same antigen-specific receptors

A

clonal selection

126
Q

The resulting family of identical cells descended from the same ancestor cell are called

A

clones

127
Q

to that antigen, clone formation is the

A

primary humoral response

128
Q

Most of the B cell clone members, or descendants, become

A

plasma cells

129
Q

B cell clone members that do not become
plasma cells become long-lived

A

memory cells

130
Q

Memory cells are responsible for the

A

immunological memory

131
Q

are produced much faster, are more prolonged, and are more effective than the events of the primary response because all the preparations for this attack have already been made

A

secondary humoral responses

132
Q

the ability of the immune system to respond more rapidly and effectively to pathogens that have been encountered

A

immunological memory

133
Q

When your B cells encounter antigens and produce antibodies against them, you are exhibiting

A

active immunity

134
Q

which may intensify the immune
response at later meetings with the same antigen,
are also available

A

booster shots

135
Q

a phenomenon in which
a population of people are generally protected
because most of a given population is immune to a
disease or infection

A

herd immunity

136
Q

the antibodies are obtained from the serum of an immune human or animal donor

A

Passive immunity

137
Q

is conferred naturally on a fetus when the mother’s antibodies cross the placenta and enter the fetal circulation, and after birth during breastfeeding

A

Passive immunity

138
Q

artificially conferred when a person receives immune serum or gamma globulin (donated antibodies)

A

Passive immunity

139
Q

is commonly administered after exposure to hepatitis.

A

Gamma globulin

140
Q

used for such purposes are descendants of a single cell and are pure antibody preparations that exhibit specificity for one, and only one, antigen

A

Monoclonal antibodies

141
Q

used for early cancer diagnosis and to track cancers hidden deep within the body

A

Monoclonal antibodies

142
Q

Humoral Immunity- Infection; contact with pathogen

A

Active- Naturally acquired

143
Q

Humoral Immunity- Vaccine; dead or attenuated pathogens

A

Active- Artificially acquired

144
Q

Humoral Immunity- Antibodies passed from mother to fetus via placenta; or to infant in her milk

A

Passive- Naturally acquired

145
Q

Humoral Immunity- Injection of donated antibodies (gamma globulin)

A

Active- Artificially acquired

146
Q

also referred to as immunoglobulins (Igs), constitute the gamma globulin part of blood proteins

A

Antibodies

147
Q

are soluble proteins secreted by activated B cells or by their plasma-cell offspring in response to an antigen, they are capable of binding specifically with that antigen.

A

Antibodies

148
Q

When the four chains are combined, the antibody molecule formed has two identical halves, each consisting of a heavy and a light chain, and the molecule as a whole is commonly described as being

A

Y-shaped

149
Q

Each of the four chains forming an antibody had a

A

variable (V) region and constant
(C) region

150
Q

uniquely shaped to “fit” a specific antigen

A

antigen-binding site

151
Q

Y-shaped structured, monomers

A

IgD, IgG, IgE

152
Q

IgM antibodies are called

A

pentamers

153
Q

IgA antibodies occur in both

A

monomer and dimers

154
Q

is the most abundant antibody
in blood plasma and is the only type that can cross the placental barrier

A

IgG

155
Q

only can fix complement

A

IgM and IgG

156
Q

dimers, is found mainly in secretions
that bathe body surfaces, such as mucus and tears.

A

IgA

157
Q

antibodies are the
“troublemaker” antibodies involved in allergies.

A

IgE

158
Q

Attached to B cell; free in
plasma, When bound to B cell membrane,
serves as antigen receptor; first
Ig class released by plasma
cells during primary response;
potent agglutinating agent; fixes
complement.

A

IgM

159
Q

Almost always attached to
B cell, Believed to be cell surface receptor
of immunocompetent B cell;
important in activation of B cell.

A

IgD

160
Q

Most abundant antibody in
plasma; represents 75–85%
of circulating antibodies,
Main antibody of both primary
and secondary responses;
crosses placenta and provides
passive immunity to fetus; fixes
complement.

A

IgG

161
Q

Secreted by plasma
cells in skin, mucosae
of gastrointestinal and
respiratory tracts, and tonsils,
Binds to mast cells and basophils
and triggers release of histamine
and other chemical mediators of
inflammation and some allergic
responses.

A

IgE

162
Q

Antibodies inactivate antigens in a number of ways

A

by complement fixation, neutralization, agglutination, opsonization,
and precipitation

163
Q

chief antibody ammunition used against cellular antigens, such as bacteria or mismatched red blood cells

A

Complement

164
Q

occurs when antibodies bind to specific sites (usually at or close to the site where a cell would bind) on bacterial exotoxins (toxic chemicals secreted by bacteria) or on viruses that can cause cell injury

A

Neutralization

165
Q

can be cross-linked into large lattices

A

antigen-antibody complexes

166
Q

When the cross-linking involves cell-bound antigens, the process causes clumping of the foreign cells, a process called

A

agglutination

167
Q

This type of antigen-antibody reaction occurs when mismatched blood is transfused

A

agglutination

168
Q

When the cross-linking process involves soluble antigenic molecules, the resulting antigen antibody complexes are so large that they become insoluble and settle out of solution.

A

precipitation

169
Q

antigen molecules are much more
easily captured and engulfed by the body’s phagocytes than are freely moving antigens.

A

agglutinated bacteria and immobilized
(precipitated)

170
Q

cells secrete their anti body “weapons,”

A

B cells

171
Q

cells fight their anti gens directly

A

T cells

172
Q

are activated to form a clone by binding
with a “recognized” antigen

A

T cells

173
Q

are not able to bind with free antigens. Instead, the antigens must be “presented” by a macrophage.

A

T cells

174
Q

Two types that are involved in the
activation process are called

A

helper T cells and cytotoxic T cells

175
Q

T cell must recognize the antigen fragment presented by the APC

A

“nonself,”

176
Q

T cell must recognize this by coupling with a specific glycoprotein on the APC’s surface at the same time

A

“self,”

177
Q

is now known to be essential for the activation and clonal selection of T cells

A

antigen presentation

178
Q

chemicals released by macrophages and dendritic cells also play important roles in the immune response

A

Cytokine

179
Q

specialize in killing virus-infected, cancer, or foreign graft cells directly

A

Cytotoxic T cells

180
Q

enters the foreign cell’s plasma membrane, delivering the so-called lethal hit

A

perforin

181
Q

pores appear in the target cell’s membrane, allowing to enter and kill the foreign cell

A

granzymes

182
Q

are the T cells that act as the “directors” or “managers” of the adaptive immune response

A

Helper T cells

183
Q

A proposed mechanism by which cytotoxic T cells kill target cells.

A
  1. Cytotoxic T cell binds tightly to the foreign target cell.
  2. Cytotoxic T cell releases perforin and granzyme molecules from its granules by exocytosis
  3. Perforin molecules insert into the target cell membrane and form pores similar to those produced by complement activation.
  4. Granzymes enter the target cell via the pores and degrade cellular contents.
  5. The cytotoxic T cell detaches and searches for another prey.
184
Q

The helper T cells also release a
variety of cytokines that act indirectly to rid the body of antigens by

A
  1. stimulating cytotoxic T cells and B cells to grow and divide
  2. attracting other types of protective white blood cells, such as neutrophils, into the area; and
  3. enhancing the ability of macrophages to engulf and destroy microorganisms
185
Q

(formerly called suppressor T cells), release chemicals that suppress the activity of both T and B cells

A

regulatory T cells

186
Q

are vital for winding down and stopping the immune response after an antigen has been successfully inactivated or destroyed.

A

regulatory T cells

187
Q

are tissue grafts transplanted from
one site to another in the same person.

A

Autografts

188
Q

are tissue grafts donated by a genetically identical person, the only example being
an identical twin.

A

Isografts

189
Q

are tissue grafts taken from a person other than an identical twin.

A

Allografts

190
Q

are tissue grafts harvested from a different animal species, such as a porcine (pig) heart valve transplanted into a human.

A

Xenografts

191
Q

Treatment that lowers the activity of the body’s immune system. This reduces its ability to fight infections and other diseases, such as cancer

A

immunosuppressive therapy

192
Q

is the most frequent cause of death in these patients

A

Explosive infection

193
Q

are abnormally vigorous immune responses in which the immune system causes tissue damage as it fights off a perceived “threat” that would otherwise be harmless to the body

A

Allergies, or hypersensitivities

194
Q

Sensitization stage

A
  1. Antigen (allergen) invades body.
  2. Plasma cells produce large amounts of class IgE antibodies against allergen.
  3. IgE antibodies attach to mast cells in body tissues (and to circulating basophils).
195
Q

secondary response

A
  1. More of same allergen invades body.
  2. Allergen binding to IgE on mast cells triggers release of histamine (and other chemicals).
  3. Histamine causes blood vessels to dilate and become leaky, which promotes edema; stimulates release of large amounts of mucus; and causes smooth
    muscles to contract.
196
Q

starts with the release of a flood of histamine when IgE antibodies bind to mast cells.

A

secondary response

197
Q

causes small blood vessels in the area
to become dilated and leaky and is largely to blame for the best-recognized symptoms of allergy

A

Histamine

198
Q

Over-the-counter (OTC) anti-allergy drugs contain

A

antihistamines

199
Q

most common type of allergy

A

immediate hypersensitivity, or acute hypersensitivity

200
Q

is fairly rare, the bodywide, or systemic, acute allergic response known as

A

anaphylactic shock

201
Q

occurs when the allergen directly enters the blood and circulates rapidly through the body, as might happen with certain bee stings, spider bites, or an injection of a foreign substance (such as horse serum, penicillin, or other drugs that act as hap tens) into susceptible individuals

A

anaphylactic shock

202
Q

Food allergies (peanut or wheat allergies) may also trigger

A

anaphylaxis

203
Q

found in emergency EpiPen® shots,
is the drug of choice to reverse these histamine mediated effects.

A

Epinephrine

204
Q

mediated mainly by a special subgroup of helper T cells, cytotoxic T cells, and macrophages, take much longer to appear (1 to 3 days) than any of the acute reactions produced by antibodies.

A

Delayed hypersensitivities

205
Q

The most familiar examples of delayed hypersensitivity reactions are those classed as

A

allergic contact dermatitis,

206
Q

happens when the body’s natural defense system can’t tell the difference between your own cells and foreign cells, causing the body to mistakenly attack normal cells.

A

autoimmune disease

207
Q

which systematically destroys joints

A

Rheumatoid arthritis (RA)

208
Q

which impairs communication between nerves and skeletal muscles

A

Myasthenia gravis

209
Q

which destroys the white matter (myelin sheaths) of the brain and spinal cord

A

Multiple sclerosis (MS)

210
Q

in which the thyroid gland produces excessive amounts of thyroxine in response to autoantibodies thatmimic TSH

A

Graves’ disease

211
Q

which destroys pancreatic beta cells, resulting in deficient production of insulin

A

Type 1 diabetes mellitus

212
Q

a systemic disease that occurs mainly in young women and particularly affects the kidneys, heart, lungs, and skin

A

Systemic lupus erythematosus (SLE)

213
Q

a severe impairment of kidney function due to acute inflammation

A

Glomerulonephritis

214
Q

may appear as a result of gene mutations that change the structure of self-proteins or as a result of alterations in self-proteins by hapten attachment or by bacterial or viral damage.

A

“new” self-antigens

215
Q

causing damage to both the heart muscle and its valves, as well as to the joints and kidneys

A

rheumatic fever

216
Q

The most devastating congenital condition in which there is a marked deficit
of both B and T cells.

A

severe combined immunodeficiency
disease (SCID)

217
Q

include both congenital and acquired conditions in which the production or function of immune cells or complement is
abnormal.

A

immunodeficiencies

218
Q

the most important and most devastating of the acquired immunodeficiencies, cripples the immune system by interferingwith the activity of helper T cells

A

acquired immune deficiency syndrome (AIDS).

219
Q

fungal brain infection

A

cryptococcal meningitis

220
Q

an eye infection

A

cytomegalovirus retinitis

ANAPHY LECTURE (10 decks)

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