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Patho > L5 > Flashcards

L5 Flashcards

1
Q

Immune responses that are normally protective, are also capable of ?

A

causing tissue injury.

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2
Q

The immune system’s homeostasis (balance) can sometimes be disrupted on its own, leading to three possible outcomes: ?

A
  • It may over-react to antigens, causing allergies.
  • It may under-react, as with human immunodeficiency virus (HIV) infection.
  • It may react to self-proteins, as in autoimmune diseases.
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3
Q

What is Harpersensitivity?

A

Def: A state of altered reactivity in which the body reacts with
an exaggerated immune response to a foreign agent

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4
Q

In Hypersensitivity, what is the response range?

A

The responses range from discomforts (as itching of skin), to
disabling or fatal diseases (bronchial asthma and anaphylaxis)

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5
Q

Injurious immune reactions are grouped under hypersensitivity,
and the resulting diseases are called ?

A

hypersensitivity diseases.

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6
Q

Hypersensitivity is elicited by ?

A

exogenous or endogenous antigens.

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7
Q

What is the Hypersensitivity types?

A

Type I, type II, type III, type IV.
Type I and II and III they are antibody meditated
Type IV are cell mediated

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8
Q

Immediate (type I) hypersensitivity, give me examples of the disorder?

A

Anaphylaxis; allergies; bronchial asthma
(atopic forms)

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9
Q

Antibody-mediated (type II)
hypersensitivity give me examples of the disorder?

A

Autoimmune hemolytic anemia;
Goodpasture syndrome

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10
Q

Immune complex-mediated (type III)
hypersensitivity give me example of the disorder?

A

Systemic lupus erythematosus;
glomerulonephritis; serum sickness;
Arthus reaction

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11
Q

Cell-mediated (type IV)
hypersensitivity give me example of the disorder?

A

Contact dermatitis; multiple sclerosis;
type I diabetes; transplant rejection;
tuberculosis

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12
Q

Immunologic Tolerance?

A

Def: Self-tolerance refers to lack of immune
responsiveness to one’s own tissue antigens.
A state of unresponsiveness to an antigen is induced by
exposure of specific lymphocytes to that antigen

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13
Q

Normal persons are?

A

Normal persons are unresponsive (tolerant) to their own
(self) antigens (auto-Ag).

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14
Q

Mechanisms of self tolerance:

A

• During development of T lymphocytes and B lymphocytes
different antigen receptors are randomly generated
• Most of the receptors that can recognized self antigens are
concealed
• Some of those receptors with self-reactivity are not concealed

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15
Q

There are mechanisms that act against self-reactivity and
prevent immune reactions against the body’s own antigens:
• Two mechanisms:

A

(1) Central tolerance
(2) Peripheral tolerance

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16
Q

(1) Central Tolerance:

A

• Deletion (death by apoptosis) of self-reactive T lymphocytes and B lymphocytes during their maturation in central (generative) lymphoid organs • i.e. T cells in the thymus and B cells in the bone marrow.

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17
Q

This deletion of self reactive immature T lymphocytes is known
as?

A

negative selection

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18
Q

• Some CD4+ T cells survive and develop into regulatory T cells
• Regulatory T cells:?

A

A population of T lymphocytes function to
prevent immune reactions against self antigens.

• Regulatory T cells develop mainly in the thymus, but they also may
develop in peripheral lymphoid tissues

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19
Q

Some self-reactive B lymphocytes are not deleted, instead
undergo a process called ?

A

receptor editing.

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20
Q

Receptor editing:?

A

a second round of rearrangement of antigen
receptor genes and expression of new receptors that are no
longer self-reactive

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21
Q

Is all self antigens are present in the thymus or bone marrow ?

A

Central tolerance is imperfect!
• Not all self antigens are present in the thymus or bone marrow
• Henceلذلك some lymphocytes with receptors for
autoantigens escape into the periphery.
• Self-reactive lymphocytes that escape negative
selection can cause tissue injury unless they are
eliminated or muzzled in the peripheral tissues.

22
Q

Peripheral Tolerance ?

A

Inactivation of auto-reactive lymphocytes in the peripheral lymphoid tissues

23
Q

Peripheral Tolerance:
Inactivation of auto-reactive lymphocytes in the peripheral
lymphoid tissues by one of three methods:

A

by one of three methods:
(i) Anergy: functional inactivation of lymphocytes rendering
them anergic ie. cannot respond to the self antigen
(ii) Suppression by regulatory T cells
(iii)Deletion of lymphocytes by apoptosis.
Sequestration of auto-Ags in immune-privileged sites: some
self antigens are hidden (sequestered) from the immune
system and do not communicate with the blood and lymph, like
some antigens in the testis, eyes, and brain.

24
Q

Autoimmunity defined as:?

A

immune reactions against self
“auto” antigens because of failure (break down) of self-
tolerance.

25
Q

Autoimmune diseases are associated with ?

A

high-affinity
autoantibodies

26
Q

Antibodies cause?

A

pathologic reactions

27
Q

Activated pathogenic self-reactive T lymphocytes…?

A

are
identified in some of autoimmune diseases

28
Q

Autoimmune diseases can be: ?2

A

1-Oregon specific
2-Systemic

29
Q

Autoimmune diseases may be:
Organ-specific:?

A

The immune responses are directed against one particular organ
or cell type and result in localized tissue damage

30
Q

Autoimmune diseases may be: systemic ?3

A

• Lesions in many organs .
• When caused by immune complexes and autoantibodies, the
lesions principally affect the connective tissues and blood vessels
of the involved organs.
• Hence the name collagen vascular diseases or connective tissue
diseases

31
Q

example of systemic autoimmune disease?

A

Systemic lupus erythematosus

32
Q

Example of specific organ autoimmune disease?

A

Diseases meditated by T cells, type I diabetes mellitus

33
Q

Mechanisms of Autoimmunity
Genetic Factors: ?4

A

• Autoimmune diseases have a tendency to run in families
• There is a greater incidence of the same autoimmune
disease in monozygotic than in dizygotic twins
• Expression of a particular MHC susceptibility genes.
• Several autoimmune diseases are linked to the HLA locus,
especially class II alleles (HLA-DR, HLA-DQ).

34
Q

Environmental Factors:
Role of microbes: ?

A

• Microbial infections  tissue necrosis and inflammation
 stimulate expression of co-stimulatory molecules on
APCs in the tissues  break down of T cell tolerance and
subsequent T cell activation.

35
Q

• Viruses and other microbes may share cross-reacting
epitopes with self antigens responses induced by the
microbe may extend to self tissues, a phenomenon called ?

A

molecular mimicry

36
Q

Example of immunologic cross-reaction is?

A

rheumatic heart disease: antibody response against streptococcus bacteria
cross-targets cardiac antigens

37
Q

Local tissue injury for any reason may lead to?

A

the release of self antigens and autoimmune responses

38
Q

Some environmental insults can altered the display of
tissue antigens
Example:?

A

• Ultraviolet (UV) radiation causes cell death  exposure of nuclear antigens  pathologic immune responses (eg. lupus flares with exposure to sunlight)

• Smoking may lead to chemical modification of self antigens (eg. In Rheumatoid arthritis).

39
Q

Gender bias of autoimmunity:?

A

• More common in females
• underlying mechanisms are not well understood, but may involve the
effect of hormones

40
Q

Graft Rejection?

A

Definition: Rejection is a process in which T lymphocytes and antibodies
produced against graft antigens react against and destroy the grafts.

41
Q

What is the Allografts:?

A

are grafts exchanged between individuals of the same species

42
Q

What happend Following transplantation ?

A

the recipient’s T cells recognize donor antigens
from the graft (the allogeneic antigens, or alloantigens)

43
Q

Rejection classification:?3

A

1) Hyperacute rejection

2) Acute rejection

3) Chronic rejection

44
Q

1) Hyperacute rejection:
• Mediated by? and occurs in (time) ?

A

• Mediated by preformed antibodies specific for antigens on graft endothelial cells.
• Occurs immediately

45
Q

2) Acute rejection
• Mediated by? and occurs in (time) ?

A

• Mediated by T cells and antibodies that are activated by alloantigens in the graft.
• occurs within days or weeks after transplantation
• Has 2 types:
I. acute cellular rejection: mediated by CD8+ and CD4+ T lymphocytes
II. acute humoral rejection: antibody-mediated

46
Q

Chronic rejection:
• Mediated by? and occurs in (time) ?

A

• Mediated by T cells that react against graft alloantigens and secrete cytokines
• Indolent, occurs over months or years

47
Q

Rejection clinical outcome:?

A

Hyperacute rejection:
Ischemic necrosis of the graft

Acute rejection:
Early graft failure

Chronic rejection:
Progressive loss of graft function

48
Q

Graft-Versus-Host Disease?

A

Definition: GVHD occurs when immunologically competent cells or their
precursors are transplanted into immunologically crippled recipients, and
the transferred cells recognize alloantigens in the host and attack host
tissues.

49
Q

Graft-Versus-Host Disease Clinical outcome:?2

A

oAcute: target organs: liver, skin, and gut  jaundice, and mucosal
ulceration  bloody diarrhea
Cutaneous involvement  rash first on the neck, ears, and palms of the
hands and soles of the feet and then becomes generalized.

oChronic: skin lesions resembling those of systemic sclerosis and other
autoimmune disorders.

50
Q

Immunodeficiencies disorders?

A

• Immunodeficiencies are manifested clinically by increased infections,
which may be newly acquired or reactivation of latent infections

51
Q

Immune deficiencies can be classified, according to etiology, into:?

A

1) Primary (or congenital): genetically determined:
I. Defects in Leukocyte Function
II. Defects in the Complement System
2) Secondary (or acquired): as complications of cancers, infections (eg
AIDS), malnutrition, or side effects of immunosuppression, irradiation, or
chemotherapy for cancer and other diseases

Patho (11 decks)

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