Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immune Exam 3 > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

immediate hypersensitivity

A

type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

antibody dependent hypersensitivity

A

type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

immune complexes hypersensitivity

A

type III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cell mediated hypersensitivity

A

type IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

allergies/ anaphylaxis hypersensitivity

A

type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

anti-cell surface antigen reactions hypersensitivity

A

type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

accumulation of immune complexes hypersensitivity

A

type III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

delayed hypersensitivity

A

type IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

IgE mediated hypersensitivity

A

type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

IgM and IgG hypersensitivity

A

type II & III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T cell mediated hypersensitivity

A

type IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

mast cell degranulation hypersensitivity

A

type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

complement mediated hypersensitivity

A

type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

activated macrophage hypersensitivity

A

type IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

immune complex deposition hypersensitivity

A

type III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

cells involved in type I hypersensitivity

A
  • mast
  • basophils
  • eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

preformed mediators type I hypersensitivity

A
  • histamine
  • ECF-A
  • heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Secondary mediators type I hypersensitivity

A
  • PAF
  • leukotrienes
  • prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

reaction site type I hypersensitivity

A

local

systemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Reactions type I hypersensitivity

A

hay fever
asthma
anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

disease in which immune response to allergen leads to tissue damage and organ dysfunction

A

allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

clinical manifestation of type I hypersensitivity like asthma, eczema, hay fever, allergy

A

atopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

people who suffer from immediate hypersensitivity

A

atopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

reaction resulting in vasodilation and construction of smooth muscle

A

anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

most common clinical allergy

A

allergic rhinitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

where is allergic rhinitis localized?

A

nasal mucosa

conjunctiva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

IgE mediated, BHR, bronchus

A

asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

common skin disorder

A

atopic dermatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

substance that gives rise to immediate hypersensitivity

A

allergen, antigen, Ag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

physical properties of allergen

A
  • most proteins
  • small
  • soluble
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how are allergens classified?

A

routes of exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

IgE

A
  • monomer
  • low concentration
  • short half life
  • eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

is there placental transfer in IgE?

A

virtually none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Phases of type I hypersensitivity

A

sensitization

triggering phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

acute reaction, allergen + IgE

A

anaphylactic reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

acute reaction, no allergens or IgE, codeine, morphine

A

anaphylactoid reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fatal laryngeal edema

A

reaction to penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Urticaria

A

vascular reaction

increased vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

urticaria characterized by

A

erythema

wheal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

common cause of urticaria

A

allergy
infection
stress

41
Q

asthma routes

A

chemotactic factor

spasmogens (broncho constriction)

42
Q

chemotactic factors

A

IL-5

TNFa

43
Q

spasmogens

A

histamine
leukotrienes
prostaglandins

44
Q

one parent allergy

A

30%

45
Q

two parents allergy

A

50%

46
Q

diagnostic type I hypersensitivity

A

skin test
ELISA
pulmonary function

47
Q

skin tests

A

wheal and flare

time course

48
Q

EIA

A
  • measure IgE
  • used in place of skin tests
  • medication may interfere
  • unstable heart condition
49
Q

treat type I hypersensitivity

A
  • avoid allergen
  • antihistamine
  • corticosteroid
  • mast cell stabilizer
  • leukotriene inhibitor
  • nasal anticholinergics
  • immunomodulators
  • epinephrine
  • B2 agonists
  • methylxanthines
50
Q

hyposensitization

A

inject allergy + adjuvant over period of months

51
Q

goal of hyposensitization

A

shift TH2 (IgE) to Th1 (IgG)

52
Q

types of immunotherapy type I hypersensitivity

A

SCIT
SLIT
OIT

53
Q

T cells type I hypersensitivity

A
  • suppress IgE (IFNy, IL-12)
54
Q

IgE is dependent on what?

A

T cells

Th2: IL-4, IL-5, IL-10

55
Q

Contact dermatitis

A

type IV hypersensitivity

56
Q

Serum sickness

A

type III hypersensitivity

57
Q

glomerulonephritis

A

type III hypersensitivity

58
Q

direct target hypersensitivity

A

type II

59
Q

reactions in type II hypersensitivity

A
  • complement
  • ADCC
  • anti-receptor antibodies
60
Q

Blood transfusion

A

type II hypersensitivity

61
Q

erythroblastosis fetalis

A

type II hypersensitivity

62
Q

transplant rejection

A

type II hypersensitivity

63
Q

ADCC

A

antibody IgM or IgG

  • against self
  • against foreign
64
Q

ABOs

A

develop abs without prior sensitization

can occur on first transfusion

65
Q

joint and heart valve damage

A

rheumatic fever

66
Q

destruction of platelets

A

thrombocytopenia

67
Q

acetylcholine receptors on muscle cells

A

myasthenia gravis

68
Q

type II reaction target tissues

A 
Rheumatic fever
thrombocytopenia
MG
good pasture
Graves
MS
69
Q

where do antibodies collect in good pastures?

A

kidney glomerulus

lung alveoli

70
Q

drug induced reactions

A

type II

71
Q

blood vessel dilation, sneezing, cough

A

type III hypersensitivity

72
Q

Examples of type III hypersensitivity

A

arthus
acute serum sickness
autoimmune

73
Q

immune processes in type III hypersensitivity

A

complement

phagocytic cells

74
Q

repeated exposure to ags

A

inhale antigenic material

75
Q

vasodilation and bronchoconstriction

A

type III hypersensitivity

76
Q

vasodilators

A

type III hypersensitivity

77
Q

phases of type III hypersensitivity

A

immune complex form

deposition

78
Q

large or small immune complexes cleared faster?

A

larger

79
Q

what affect complex clearance

A 
ag class
glycosylation
80
Q

where does deposition of immune complexes occur

A

high bp

bifurcations

81
Q

what may cause increased deposition in kidney of immune complexes?

A

charge (+)

82
Q

what solubilizes complexes?

A

complement

83
Q

what cause of exacerbate immune complex disease?

A

Cā€™ deficiencies

84
Q

Serum sickness

A
  • after injection of foreign protein

- large aggregates

85
Q

cell mediated hypersensitivity

A

type IV

86
Q

CD4 hypersensitivity

A

delayed

87
Q

CD8 hypersensitivity

A

cytotoxic

88
Q

how does type IV hypersensitivity differ?

A
  • t cell activated macrophages mediate

- starts after latent period of several hours

89
Q

when does type IV hypersensitivity peak?

A

48-72 hours

90
Q

Hapten

A

small
lipophilic
penetrate epidermis

91
Q

what conjugate to self proteins?

A

hapten

92
Q

neo-antigen

A

hapten + protein

93
Q

eczematous reaction

A

contact hypersensitivity

72 hours

94
Q

skin injected with soluble ag

A

tuberculin type hypersensitivity

72 hours

95
Q

Most serious type of type IV hypersensitivity

A

granulomatous hypersensitivity

21-28 days

96
Q

three types of type IV hypersensitivity

A
  • contact
  • tuberculin
  • granulomatous
97
Q

What decreases cytokine production in contact hypersensitivity

A

prostaglandin

98
Q

diagnosis of contact hypersensitivity

A

patch test

99
Q

Tuberculin type IV hypersensitivity

A
  • hardening and swelling of injected area

- lesions resolve in 1 week

Immune Exam 3 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions