HYPERSENSITIVITY Flashcards

1
Q

immune responses can also have deleterious effects on the body

T/F

A

T

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2
Q

immune responses may eradicate the infecting microorganism and at the same time, they can cause- significant tissue damages.

T/F

A

T

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3
Q

To distinguish between the beneficial and deleterious effects of the immune responses, the term _________ is used to describe an ______ response that causes ________ in a host

A

hypersensitivity

exaggerated

tissue damage

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4
Q

Hypersensitivity Reactions

Such a response usually occurs in a sensitized host when it encounters the same antigen for the ______ time.

A

second

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5
Q

There are four types of Hypersensitivity Reactions

Type I: ________

Type II: _________

Type III: __________

Type IV: _________

A

Anaphylactic

Cytotoxic

Immune Complex Disorders

Delayed Hypersensitivity

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6
Q

The first three hypersensitivity reactions are _______ mediated, whereas type IV hypersensitivity involves _______ and ________.

A

antibody

T cells and macrophages

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7
Q

Type 1 Hypersensitivity

Aka ___________

Effector cells are ???

Immuno- globulin???

Complement activation?

A

anaphylactic hypersensitivity

Basophils Mast Cells

IgE

No

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8
Q

Type 2 Hypersensitivity

Aka ___________

Immuno- globulin???

Complement activation?

A

cytotoxic antibody

IgG or IgM

Yes

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9
Q

Type 3 Hypersensitivity

Aka ___________

Immuno- globulin???

Complement activation?

A

Immune complex disorders

IgG or IgM

Yes

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10
Q

Type 4 Hypersensitivity

Aka ___________

Effector cells??

Complement activation?

A

delayed-type hypersensitivity

T cells, macrophages
No

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11
Q

Type 1 hypersensitivity

It is also known as immediate hypersensitivity because _________

A

the reaction occurs within minutes of contact with the antigen or allergen.

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12
Q

Type 1 hypersensitivity

An individual has circulating ______ or tissue ______-cells that are sensitized by the cytotropic antibody, _____.

Upon subsequent exposure to the allergen, these sensitized cells are triggered to release ________ that produce allergic symptoms.

A

basophils

mast; IgE

vasoactive amines

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13
Q

Mechanism of Vasoactive Amine Release

The effector cells involved in an allergic response are _______ and ______ .

In general, ______ are found in circulation, whereas ______ are distributed in the tissues.

A

basophils and mast cells.

basophils; mast cells

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14
Q

Mechanism of Vasoactive Amine Release

The two cell types (basophils and mast cells) are indistinguishable in many of their biologic characteristics:

They express cell surface ____- receptors for ______

They have cytoplasmic granules containing __________
.
They are triggered to release vasoactive amines by similar mechanisms.

A

Fc; IgE

vasoactive amines

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15
Q

Mechanism of Vasoactive Amine Release

IgE antibodies produced by the plasma cells are bound to the ______ of a ____________ by way of ______ receptors.

Subsequent exposure to the same allergen will cause ________ formation on the cell surface, leading to the release of vasoactive amines.

A

cell surface

basophil or mast cell

Fc

immune complex

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16
Q

Mechanism of Vasoactive Amine Release

The crucial event appears to be ________ of the effector cell surface ____ receptors.

A

cross-linking

Fc

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17
Q

Mechanism of Vasoactive Amine Release

At least ____ IgE molecules are occupying the ______ Fc receptors on an effector cell, and the allergen is _____valent, such that it is able to ________________ on the effector cell.

A

two

adjacent

multi

cross- link the two IgE molecules

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18
Q

Mechanism of Vasoactive Amine Release

One the biologic events resulting from receptor cross-linking is the fusion of _________ and ______, which leads to release of stored, preformed granular contents (the ________ cells become _________).

A

granular membranes and cell membranes

effector

degranulated

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19
Q

Mechanism of Vasoactive Amine Release

Whereas the released vasoactive amines cause ______ symptoms of an allergic response, the _________ convey the specificity of an allergic re sponse.

A

general

IgE molecules

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20
Q

Type 1 hypersensitivity

Receptor cross-linking also results in the synthesis of mediators from arachidonic acid

T/F

A

T

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21
Q

Allergens are the ______ that are able to elicit __________ responses in certain individuals.

A

antigens

IgE antibody

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22
Q

Most naturally occurring allergens have a molecular weight of ______ to ________ daltons.

A

10,000 to 70,000

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23
Q

Small antigens may not have sufficient numbers of _______ to facilitate the __________ to trigger a basophil or mast cell degranulation.

while a larger molecule may not be able to ____________________ to reach the sensitized effector cells.

A

epitopes

Fc receptor cross-linking

diffuse, across the mucosal surface

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24
Q

Various modes of exposure to allergens are identified:

  1. The ________ is constantly exposed to airborne particles that may cause allergic responses. The most common inhalant allergens are plant pollens, fungal spores, and animal danders.

2.Absorption of allergen from the _______ can also cause allergic responses.

  1. Direct _______ with pollen or other allergen can cause _______ or even _______ symptoms in a highly sensitive individual.
A

respiratory airway

digestive tract

skin contact

localized urticaria

systemic

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25
Q

Classification of the Mediators of the allergic response

The mediators of allergic response may be divided into two categories:

_______-formed mediators
_________formed mediators

A

Pre

Newly

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26
Q

Classification of the Mediators of the allergic response
The mediators of allergic response may be divided into two categories:

Pre-formed mediators; ______ in the ________

Newly formed mediators; _____ after the cells are _________.

A

stored; granules

synthesized; triggered

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27
Q

Histamine

Histamine causes _____ of the bronchioles and smooth muscle of blood vessels, _____eases capillary permeability, and _____eases mucous gland secretion in the airway.

A

contraction

incr; incr

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28
Q

Histamine

This ____-formed mediator is stored in the granules and can be released _________ after allergen-antibody reaction.

A

pre

1 to 2 minutes

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29
Q

Histamine

The duration of histamine activity is approximately __________

A

10 minutes.

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30
Q

Eosinophil chemotactic factor of anaphylaxis

This is a _____ formed mediator released during _______.

A

pre; degranulation

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31
Q

Eosinophil chemotactic factor of anaphylaxis

It stimulates ________ to migrate to the site of an antigen-antibody reaction.

A

eosinophils

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32
Q

Eosinophil chemotactic factor of anaphylaxis

Eosinophils are known to have several functions, which include
(1)___________ of ________complexes
(2) release of the enzymes ______ and ______ . These enzymes ______ the allergic reaction caused by allergens.

A

phagocytosis

antigen-antibody

histaminase and arylsul fatase

dampen

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33
Q

Arachidonic acid

This is liberated from the ________ by the action of the enzymes ______,_______, and _________

A

membrane lipid

phospholipase A or phospholipase C and diacylglycerol lipase.

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34
Q

Arachidonic acid

The freed arachidonic acid is then processed by the __________ pathway, or the _______ pathway.
leading to __________ production, the latter leads to __________ production.

A

cyclooxygenase

lipoxygenase

prostaglandin

leukotriene

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35
Q

Prostaglandin D2 causes vaso_________ and ____eases vascular permeability.

A

dilation

incr

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36
Q

Prostaglandin D2

The clinical symptoms caused by this compound are similar to those seen with histamine-__________ ——- and ———- reaction.

A

erythematous

wheal and flare

37
Q

Prostaglandin D2

However, the prostaglandin D2 effect can persist for as long as __________; the histamine effect lasts approximately __________.

A

2 hours

10minutes

38
Q

Leukotrienes C4, D4 or E4 cause ______ and ______ formation.

When inhaled, they cause broncho______.

A

erythema and wheal

spasm

39
Q

Leukotrienes C4, D4 or E4

Their bronchoconstrictic potency is ____ to _______ times that of histamine.

A

30 to 1000

40
Q

Leukotrienes C4 and D4 have also been shown to stimulate mucous secretion by human airway tissue.

T/F

A

T

41
Q

Type II hypersensitivity involves Ig___ or Ig___ antibody against cell surface molecules or tissue components.

A

G

M

42
Q

Type II hypersensitivity

The tissue damage-may be mediated by one of the following mechanisms:
(1) accelerated ___________ by the __________ system

(2) blockade of _________ because of ______________

(3)_______-mediated _____ of the target cells, or

(4) The damage of ___________________ by the _________ released by the ______ present at the site of antigen - antibody reactions.

A

clearance of the antibody–sensitized target cells ; mononuclear phagocyte

normal cellular function ; antibody binding to the target cells,

complement; lysis

innocent by-stander cells or tissue

lysosomal enzymes; neutrophils

43
Q

Type II Hypersensitivity

_______ Mediated Damage
_______ Mediated Cell Lysis
________________ to tissue components

A

Antibody

Complement

Cytotoxic antibodies

44
Q

Type II Hypersensitivity

Antibody Mediated Damage

________ anemia
_________ disease
______________

A

Hemolytic

Graves’

Myasthenia Gravis

45
Q

Type II Hypersensitivity

Complement Mediated Cell Lysis

———— reactions

_____________- _______ incompactibility

A

Transfusion

Hemolytic disease of the newborn

Rhesus

46
Q

Type II Hypersensitivity

Cytotoxic antibodies to tissue components

eg
________________

A

Goodpasture’s syndrome

47
Q

Antibody Mediated Damage : Hemolytic anemia

Hemolytic anemia is frequently associated with (cold or warm?) antibody antibody production against red cell antigen of the _____ system.

The sensitized red blood cells are cleared by the ______ at an accelerated rate, causing aneamia in the afflicted individual..

A

Warm; Rh

macrophages

48
Q

Antibody Mediated Damage: Graves Disease

Patients with Graves’ disease have circulating antibodies specific for ___________.
When bound to the __________, these antibodies will stimulate the ________________ to produce _______, independent of the normal feedback control mechanism.

Persistent simulation of the thyroid gland causes _________. These antibodies are known as _______________________

A

thyroid stimulating hormone (TSH) receptor

TSH receptors

thyroid epithelial cells ; thyroglobulin

hyperthyroidism; long-acting thyroid stimulator (LATS).

49
Q

Antibody Mediated Damage: Myasthenia Gravis

Here, antibodies against cell surface structure blocks the normal cellular activities.
The antibody against _________ prevents the neurotransmitter, ______, from binding to the receptor at the ______.

_____________ is the clinical manifestation.

A

acetylcholine receptors

acetylcholine; neuromuscular junction

Muscular paralysis

50
Q

Complement Mediated Cell Lysis

Transfusion reactions

When the antibody - antigen complex is able to activate the _________, direct cell lysis occurs.

Transfusion of ABO-incompatible blood will result in _____________ because the recipient has antibodies to non-self ABO antigens

A

complement cascade

lysis of the donor’s red blood cells

51
Q

____________ are the most important clinical manifestation of this type of hypersensitivity (Type 2)

A

Transfusion reactions

52
Q

Complement Mediated Cell Lysis

Hemolytic disease of the newborn (HDNB) is due to ________________________ incompatibility.

The ___________ antigen is the most frequently in volved red cell antigen.

A

maternal - fetal red cell

Rhesus D (RhD)

53
Q

Complement Mediated Cell Lysis

Hemolytic disease of the newborn (HDNB)

An RhD-_____ mother be comes immunized to the D antigen on fetal red blood cells because of _________ during delivery

The mother synthesizes Ig____ antibodies against the D antigen.

In a subsequent pregnancy with an RhD- ________ fetus, the Ig____ antibodies cross the placenta and circulate in fetal circulation, causing ______-mediated lysis of the fetal red blood cell.

A

negative

maternal - fetal blood mixing

G

positive; G

complement

54
Q

Cytotoxic Antibodies to Tissue Components

Cytotoxic antibodies to tissue components frequently cause _______ responses. The sequence of events includes antibody-antigen reaction, complement activation, generation of such chemotactic factors as _____ and ______, infiltration of the tissue by ________, and release of __________ , which eventually leads to tissue damage.

The classic example is ___________

A

inflammatory

C3a and C5a; neutrophils

lysosomal enzymes

Goodpasture’s syndrome.

55
Q

Good Pasture’s Syndrome

The patient develops antibodies against _______________ and ____________

The inflammatory reactions produced by anti- basement membrane antibody deposition account for the clinical symptoms observed in these patients.

The symptoms include _______,______,_______

A

glomerular and pulmonary basement membranes.

hematuria, renal failure, and hemoptysis

56
Q

Type III Hypersensitivity

Type III reactions are triggered by the ________________ in tissues, causing __________.

The antibody involved is predominantly ________ or _______

and the antigens can be infecting microorganisms, drugs, or self-antigens.

A

deposition of circulating immune complexes

inflammation

IgG or IgM,

57
Q

Type III Hypersensitivity

_________ is usually activated, which greatly _______ the __________

A

Complement

amplifies

inflammatory response.

58
Q

Fate of Circulating Immune Complexes

Under normal conditions circulating immune complexes are ________ by the ________________, preventing _________ and associated damage.

A

rapidly cleared

mononuclear phagocytic system,

tissue deposition

59
Q

Fate of Circulating Immune Complexes

(Small or Large?) immune complexes are cleared rapidly by the host,
whereas (small or large?) soluble complexes tend to have a prolonged plasma half-life and are associated with tissue deposition, which causes inflammatory responses.

A

Large

Small

60
Q

Examples of Type III Hypersensitivity

1) ______ Reaction
2._________ Disorders
3. Destruction of __________

A

Arthus

Immune Complex

Innocent Bystanders

61
Q

Examples of Type III Hypersensitivity

  1. Immune Complex Disorders
    a. _____________
    b. Vasculitis eg __________
A

Glomerulonephritis

poly artheritis nodosa

62
Q

The Arthus reaction is induced experimentally by _________ of the antigen into a ________ animal:

The local antigen-antibody interaction (________________) results in destructive inflammation of _______________, called _________

A

intradermal injection

sensitized

immune complex formation

small blood vessels

vasculitis.

63
Q

The Arthus reaction

_________ and ________ appear within __________ and subside within ___________

A

Local swelling, and erythema

1 to 2 hours

10 to 12 hours.

64
Q

The Arthus Reaction

Microscopic examination of the tissue reveals _______ infiltration initially; followed by _________ cells and _________ infiltration.

A

neutrophil

mononuclear; eosinophil

65
Q

In Arthus reaction,

The ————— and __________degrade the immune complexes.

A

mononuclear cells and eosinophils

66
Q

Immune Complex Disorders

The term immune complex disorder is used to describe the diseases associated with clinical features arising from _______________.

The classic example is __________, which frequently develops in patients who receive _________ serum as a form of _____ immunotherapy or immunosup pressive therapy.

For example, _________ to _______

A

immune complex deposition

serum sickness

heterologous; passive

horse antisera to diphtheria,

67
Q

Immune Complex Disorders

The patients make _____ against the ________ serum proteins and develop immune complex disorders.

A

antibodies

heterologous

68
Q

Immune Complex Disorders

Glomerulonephritis
Deposition of immune complex in the ________ causes inflammatory responses that present with clinical symptoms glomerulonephritis.

Vasculitis
immune complex deposition on _________ causing injury. eg _________ which is a systemic vasculitis characterized by necrotisisng inflammation that affect medium sized and small muscular arteries, limiting function and causing injury.

A

renal glomeruli

blood vessels

polyarteritis nodosa

69
Q

Type 3 hypersensitivity

Destruction of Innocent Bystanders

Circulating immune complexes can ______________ to the elements of blood, initiating their destruction and that of innocent bystanders.

A

nonspecifically adhere

70
Q

Type 3 hypersensitivity

Destruction of Innocent Bystanders

Drug administration often elicits an antibody response that results in circulating ________ immune complexes.

These completes become ______________, causing __________ hemolysis.

A

antibody-drug

adsorbed onto the surface of red blood cells

intravascular

71
Q

Type 3 hypersensitivity

Destruction of Innocent Bystanders

The absorption of immune complexes is thought to be mediated, by the red blood cell surface ______ receptors.

___________ ,________, and __________ are known to cause red blood cell lysis by this mechanism.

A

C3b

Quinidine, quinine, and phenacetin

72
Q

Type IV Hypersensitivity

Type IV hypersensitivity, a.k.a ___________ immune re action or ________ hypersensitivity

A

cell-mediated

delayed

73
Q

Type IV Hypersensitivity
Type IV hypersensitivity

is mediated by (soluble or insoluble ?) factors or ________ released by _____________

A

Soluble

lymphokines; sensitized lymphocytes.

74
Q

Type IV Hypersensitivity

The characteristic histology of the lesion is a __________ cell infiltration.

Such lesions appear _____-______ following antigen challenge and peak within _________

A

mononuclear

24 to 43 hours

72 hours.

75
Q

Type IV Hypersensitivity

Antibody and complement are usually directly involved in type IV hypersensitivity.

T/F

A

F

Antibody and complement are usually not directly involved in type IV hypersensitivity.

76
Q

Type IV Hypersensitivity: Mechanism of Pathogenesis

The response is initiated by interactions between the antigen and a small number of _____________ that produce
__________ , following their activation.

The lymphokines have biologic activities affecting various cell types, such as _______,_________, and _______
These secondary cells are recruited to the site of reaction.

The overall function of lymphokines is to amplify the response that is initiated by a (small or large?) number of ___ lymphocytes.This is achieved by _________________________________________________________________________

Normal control mechanisms lead to resolution of the reaction; however, multiple antigenic challenges in a hypersensitive individual may lead to the ______ and _______ of the lesion.

Usually the symptoms develop over a period of __________ after antigen exposure, and the histologic examination shows characteristic ___________ infiltration.

A

sensitized T lymphocytes. ; Lymphokines

macrophages, neutrophils, and other lymphocytes.

Small; T

recruiting and directing the secondary cells, macrophages, neu trophils, and other lymphocytes, both T and B cells

ulceration and- necrosis; 24 to 48 hours

mononuclear

77
Q

Examples of Type IV
Hypersensitivity Tuberculin-Type Hypersensitivity

Tuberculin-Type hypersensitivity is induced by _________ of the antigen in a __________ individual.

The area of _________ and _______ at the site of injection appears within ___________

A

subcutaneous injection; sensitized

induration and swelling

24 to 72 hours.

78
Q

Examples of Type IV
Hypersensitivity Tuberculin-Type Hypersensitivity

Microscopic examination reveals intense ________ cell infiltration around the blood vessels and disruption of the ______________ in the _________

A

mononuclear

organization of the collagen bundles in the dermis.

79
Q

Examples of Type IV
Hypersensitivity Tuberculin-Type Hypersensitivity

The classic example is the tuberculin skin test in which _____________ prepared from the culture filtrate of mycobacterium tuberculosis is administered _____________.

A

purified -protein derivative (PPD)

intradermally

80
Q

Tuberculin-Type Hypersensitivity

positive response consists of _____ or greater ______ and ________ between ___________ and _______ hours.

A

10mm

erythema and induration

48 and 72

81
Q

Tuberculin-Type Hypersensitivity

A positive test indicates that the individual has been ____________

A negative test signifies either ——————- or _____________

A

exposed to mycobacterium tuberculosis or related organisms

no infection or a false negative due to immunosuppression associated with severe infection.

82
Q

Examples of Type IV Hypersensitivity : Contact sensitivity

Certain compounds can cause systemic sensitization through ____________.

A second encounter with the same antigen by skin contact results in ____ of the ________ with formation of ________.

A

direct skin contact

edema; epidermis; microvesicles

83
Q

Examples of Type IV Hypersensitivity : Contact sensitivity

The microscopic observation of the lesion indicates a _______ cell infiltrate that first appears at 6 to 8 hours and peaks at 12 to 15 hours after exposure to the antigen.
The most common antigens that induce contact sensitivity are _______ and ______

A

mononuclear

poison ivy and poison oak.

84
Q

Examples of Type IV
Hypersensitivity Granulomatous hypersensitivity

Granulomatous hypersensitivity results from the - persistent _________________ within _____________ that the cell is ______________________

A

presence of microorganisms within the macrophages

unable to destroy.

85
Q

Inert substances, such as talc, may also cause granulomatous hypersensitivity. giant cells.

T/F

A

T

86
Q

Granulomatous hypersensitivity

The characteristic cells found in a granulomatous lesion are ___________ ,__________,__________ , which are multinucleated giant cells

A

lymphocytes

macrophages and epithelioid cells

87
Q

Epithelioid cells are(well or poorly?) understood.

A

Poorly

88
Q

Granulomatous hypersensitivity

The giant cells are _____nucleated with (little or large?) endoplasmic reticulum, ______ mitochondria, and lysosomes.

A

multi

little

degenerated

89
Q

Granulomatous hypersensitivity is seen in __________,___________ and __________

A

tuberculosis, leprosy, and sarcoidosis.