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IS LEC MIDTERMS > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

undesirable reactions produced by the normal immune system, including allergies and autoimmunity

A

Hypersensitivity

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2
Q

type I hypersensitivity

A

immediate, atopic, anaphylactic

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3
Q

type II hypersensitivity

A

antibody dependent

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4
Q

type III hypersensitivity

A

immune complex

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5
Q

type IV hypersensitivity

A

cell mediated or delayed type of hypersensitivity

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6
Q

also known as immediate or anaphylactic
hypersensitivity

A

Type I hypersensitivity

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7
Q

what are the reactions involved in type I hypersensitivity?

A

Skin (eczema), Eyes (conjunctivitis), Nasopharynx (rhinorrhea, rhinitis), Bronchopulmonary tissue (asthma), Gastrointestinal (gastroenteritis)

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8
Q

the range of symptoms in type I hypersensitivity?

A

minor inconvenience to death

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9
Q

the reaction takes ? from the time of exposure to the antigen in type I

A

15-30 minutes

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10
Q

type I delayed onset

A

6-8 hours

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11
Q

late phase reaction

A

leukotrienes

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12
Q

type I is mediated by ? antibody

A

IgE

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13
Q

primary cellular component in type I is?

A

Mast cell and Basophil

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14
Q

reaction is amplified and/ or modified by ? in type I

A

Platelets, Neutrophils and Eosinophils

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15
Q

? stimulated and release histamine?

A

Mast cells

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16
Q

mast cells stimulated and release ?

A

Histamine

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17
Q

are non-parasite antigens that can stimulate a type I hypersensitivity response

A

Allergen

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18
Q

term for the genetic trait to have a predisposition for localized anaphylaxis

A

Atopy

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19
Q

mechanism of type I

A

induce the synthesis of IgE then binds on surface of mast cell then reintroduced antigen interacts with IgE on mast cell causing cells to degranulate and release large amounts of histamine

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20
Q

produced by TH2 and upregulate production of IgE

A

IL-4

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21
Q

produced by TH1 and downregulate production of IgE

A

IFN-gamma

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22
Q

which mediator of type I

smooth muscle contraction & binds to the receptors on endothelial causes separation of junctions, increasing permeability

A

H1 receptors

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23
Q

which mediator of type I

mucus secretion and vasodilation

A

H2 receptors

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24
Q

which mediator of type I

Increases fluid secretion and peristalsis (diarrhea and vomiting)

A

degranulation in gastrointestinal tract

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25
Q

which mediator of type I

decrease in airway diameter (CONSTRICTION OF SMOOTH MUSCLE AROUND THHE BRONCHI, anaphylaxis) and mucus secretion

A

degranulation in lungs

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26
Q

which mediator of type I

increase blood flow and vascular permeability, causing edema

A

degranulation in along blood vessels

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27
Q

which mediator of type I

causes prolonged constriction of SM

A

Leukotrienes

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28
Q

which mediator of type I

can cause bronchoconstriction

A

Prostaglandins

29
Q

? do not die

A

mast cells or basophils

30
Q

? regenerate and synthesize new granules

A

degranulated cells

31
Q

diagnosis for type I

A

prick and intradermal test (skin) and measurement of total IgE (measured by ELISA)

32
Q

treatment for type I

A

Drugs
* non steroidal-inflammatories block histamin receptors
* antihistamines
* steroids
* Theophylline OR epinephrine -prolongs or increases CAMP levels in mast cells which inhibits degranulation

Immunotheraphy
* Desensitization (hyposensitization) also known as allergy shots
* Repeated injections of allergen to reduce the IgE on Mast cells and
produce IgG

  • Over an extended period, injecting increasing dose of allergen
  • Epi
33
Q

vasoconstrictor, also relaxes SM

A

Epi

34
Q

aka cytotoxic hypersensitivity and may affect variety of organs and tissue

A

type II

35
Q

exogenous chemicals which can attach to cell membranes can also lead to type II

A

Haptens

36
Q

diseases in type II

A

Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia and penicillin allergy

37
Q

reaction time of type II

A

minutes to hours

38
Q

type II is primarily mediated by antibodies of the?

A

IgM or IgG

39
Q

rhogam ? of ? and after delivery within ?

A

28 weeks of gestation, 72 hours

40
Q

diagnosis of type II

A

biopsy by immunofluorescence and staining pattern is normally smooth and linear, such as that seen in Goodpasture’s nephritis

41
Q

treatment of type II

A

anti-inflammatory and immunosuppressive agents

42
Q

type III is primarily mediated by?

A

IgG although IgM may also be involved

43
Q

if the large amount of antigen and antibody complexes in the blood are not eliminated what will happen?

A

they can deposit in capillaries or joints and trigger inflammation

44
Q

immunized rabbits with horse serum by repeated intradermal
reaction

A

Arthus

45
Q

signs and symptoms of type III with horses for diphth and tetanus (HETEROLOGOUS SERUM)

A

antisera made with horses for diphth and tetanus (HETEROLOGOUS SERUM)

46
Q

in type III the reaction may take?

A

3-10 hours after exposure

47
Q

chronic bacterial, viral or parasitic infections

A

exogenous antigens

48
Q

non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE

A

endogenous antigens

49
Q

? bind to immune complexes via FcR and phagocytize the complexes

A

polymorphonuclear leukocyte and macrophages

50
Q

polymorphonuclear leukocyte and macrophages bind to immune complexes via FcR and phagocytize the complexes BUT if unable to phagocytize the immune complexes it can cause?

A

inflammation via C activation (C3a, C4a, C5a)

51
Q

treatment for type III

A

anti-inflammatory agents

52
Q

diagnosis of type III

A

examination of tissue biopsies for deposits of immunoglobulin and complement by immunofluorescence microscopy

53
Q

pileup of pre-formed immune complexes on the basement membrane leads to lumy-bumpy deposits

A

serum-sickness

54
Q

reaction involves sensitized T-cells

A

type IV

55
Q

mediated by cells rather than abs

A

type IV

56
Q

release cytokines to activate macrophages causing inflammation and tissue damage

A

Th1 cells

57
Q

Continued macrophage activation can cause?

A

chronic inflammation resulting in tissue lesions, scarring, and granuloma formation

58
Q

response time for type IV starts after?

A

48-72 hours

59
Q

ARE ACTIVATED BY IF-GAMMA &TNF-BETA

A

macorphages

60
Q

what activates macrophages?

A

IF-GAMMA &TNF-BETA

61
Q

in VIVO diagnostic test for type IV?

A

cutaneous reaction (montoux) test and patch test (contact dermatitis)

62
Q

in VITRO diagnostic test for type IV?

A

mitogenic response, lympho- cytotoxicity and IL-2 production

63
Q

treatment of type IV

A

corticosteroids and immunosuppressive agents

64
Q

edema, serum into tissue

A

wheal

65
Q

erythema, dilation of BV

A

flare

66
Q

another diagnostic test for type IV?

A

wheal and flare for 10-15 mins

67
Q

aka allergy shots

A

desensitization

68
Q

prolongs or increases CAMP levels in mast cells which inhibits degranulation

A

Theophylline or Epinephrine

IS LEC MIDTERMS (7 decks)

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