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IS FINALS AND REMOVALS > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Heightened state of immune
responsiveness

A

Hypersensitivity

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2
Q

Cell bound antibody reacts with antigen to
release physiologically active substances

A

Hypersensitivity type 1

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3
Q

Are those in which free antibody reacts with
antigen associated with cell surface

A

Hypersensitivity type II

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4
Q

Antibody reacts with soluble antigen to form
complexes that precipitate in the tissues.

A

Hypersensitivity type III
• Antibody reacts with soluble antigen to form

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5
Q

Complement plays a major role in producing
tissue damage.

A

Hypersensitivity type 3

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6
Q

Sensitized T cells rather than antibody are
responsible for the symptoms that develop.

A

Hypersensitivity type 4

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7
Q

Immune mediators of type 1 to 4

A

Type 1 = ige
Type 2 = igg
Type 3 = igg origm
Type 4 = t cells

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8
Q

Which hypersensitivityhas complement involvement

A

Type 2 and 3

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9
Q

Mechanism of type 1 hypersensitivity

A

RELEASE OF
MEDIATORS
FROM MAST
CELLS AND
BASOPHILS

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10
Q

Hypersensitivity type 2 mechanism

A

CYTOLYSIS DUE
TO ANTIBODY
AND
COMPLEMENT

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11
Q

Hypersentivity type 3 mechanism

A

DEPOSITS OF Ag-
Ab COMLEXES

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12
Q

Hypersensitivity’s type 4 mechanism

A

RELEASE OF
CYTOKINES

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13
Q

Example oftype 1 hypersensitivity

A

ANAPHYLAXIS,
HAY FEVER,
FOOD
ALLERGIES

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14
Q

Example of type 2 hypersensitivity

A

TRANSFUSION
REACTIONS,
HDN

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15
Q

Type 3 hypersensitivity

A

SERUM
SICKNESS, SLE

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16
Q

Type 4 hypersensitivity

A

CONTACT
DERMATITIS,
TUBERCULIN
TEST

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17
Q

Antigen contact, typically low dose via mucous
membrane (respiratory, GI) → IgE production

A

Sensitization

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18
Q

Pre-formed IgE (allergens-specific) triggers
mast cell activation → mediator release

A

Elicitation

19
Q

 Can occur within seconds-minute of exposure
 Severity ranges from irritating to fatal

A

Reactions

20
Q

In type 1, Total IgE and specific antibodies are measured
by a

A

modification of enzymes immunoassay
(ELISA).

21
Q

Increased IgE levels are indicative of

A

atopic
condition.

22
Q

Type 1 teatment

A

Antihistamine, anchromolyn sodium

Leukotriene

Bronchodilators such as irsprotrenol derviatives

Thopylline

Hyposensitvity

Suppressor t cell

Igg blocing antibodies

23
Q

nhibits mast cells
degranulation, probably by inhibiting Ca++
influx.

A

Chromolyn sodium i

24
Q

elevates
cAMP-phosphodiesterase and inhibits
intracellular Ca++ release is also used to relieve
bronchopulmonary symptoms.

A

Thophylline

25
Q

• that specifically inhibits IgE
antibodies may play a role.

A

Suppressor T cells

26
Q

also known as cytotoxic hypersensitivity and
may affect a variety of organs and tissues

A

Type 2 hypersensitivity

27
Q

The
antigens are normally endogenous, although
exogenous chemicals (haptens) which can attach
to cell membranes can also lead to

A

type II
hypersensitivity.

28
Q

Can lead to type 2 hypertension

A

• Drug-induced hemolytic anemia,
granulocytopenia and thrombocytopenia

29
Q

Diagnostic test of type 2

A

detection of circulating
antibody against tissues involved and the
presence of antibody and complement in the
lesion (biopsy) by immunofluorescence.

30
Q

It is also known as immune complex
hypersensitivity.

A

Type 3 hypersensitivity

31
Q

The reaction may be general
(serum sickness) or may involve individual
organs including skin (systemic lupus
erythematosus, arthus reaction), kidney (lupus
nephritis), lung (aspergillosis), blood vessels
(polyarteritis), joints (rheumatoid arthritis) or
other organs.

A

Type 3

32
Q

Ho long is the reaction for type 3, what siit mediated by and what type of antigenis used

A

• The reaction may take 3-10 hours after exposure
to the antigen.
• It is mediated by soluble immune complexes.
They are mostly of IgG class, although IgM may
also be involved.
• They antigen may be exogenous or endogenous in
nature. The antigen is soluble and not attached
to the organ involved.

33
Q

Diagnosis of type e

A

• Diagnosis involves examination of tissue biopsies
for deposits of Ig and complement by
immunofluorescence.

• Polyethylene glycol mediated turbidity
(nephelometry), binding of C1q and Raji
cell test are utilized to detect immune
complexes.

• The immunoflurorescent staining in type III
hypersensitivity is granular. Presence of immune
complexes in serum and depletion in complement
level are also diagnostic.

34
Q

Treatment of type 3

A

Anti inflammation

35
Q

It is also known as cell mediated or delayed type
hypersensitivity.

A

Type 4 hypersensitivity

36
Q

The classical example of this hypersensitivity is
tuberculin (montoux) reaction which peaks
48hours after the injection of antigen (PPD or old
tuberculin). The lesion is characterized by
induration and erythema.

A

Type 4 hypersensitivity

37
Q

is involved in the
pathogenesis of many autoimmune and infectious
diseases and granulomas due to infections and
foreign antigens.

A

Type IV hypersensitivity

38
Q

Another delayed hypersensitivity is

A

contact
dermatitis (poison ivy, chemicals, heavy metals)
in which the lesions are more popular.

39
Q

Mechanism for type 4

A

include T lymphocytes and
monocytes and/or macrophages. Cytotoxic T cells
(Tc) cause direct damage whereas helper T (TH1)
cells secrete cytokines which activate cytotoxic T
cells and recruit and activate monocytes and
macrophages, which cause the bulk of the
damage.

40
Q

Major lymphokines involved in delayed
hypersensitivity reaction include

A

monocyte
chemotactic factor, interleukin-2, interferon,
TNF.

41
Q

Diagnostic test in type 4 hypersensitivity

A

Diagnostic test in vivo include delayed cutaneous
reaction (montoux test) and patch test (for
contact dermatitis).
• In vitro tests for delayed hypersensitivity include
mitogenic response, lympho-cytotoxicity and IL-2
production.

42
Q

Treatment fortype 4 hypersensitivity

A

Corticosteroids and other immunosuppressive
agents are used in treatment.

43
Q

Mechanism of type 4

A

Mechanism:
• The mechanism includes T lymphocytes and
monocytes and/or macrophages.
• Cytotoxic T cells (Tc) cause direct damage
whereas helper T (TH1) cells secrete cytokines
which activate cytotoxic T cells, recruit and
activate monocytes and macrophages, which
cause the bulk of the damage
• The delayed hypersensitivity lesions mainly
contain monocytes and a few T cells.

IS FINALS AND REMOVALS (5 decks)

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