Brainscape's Knowledge GenomeTM

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


See full index

SFM Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

triggered by environmental Ags, activates mast cells in an IgE-dependent manner

A

Type I Hypersensitivity

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

genetic tendency to develop allergic diseases

A

atopy

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

what are the five Type I mediators, and what are their functions?

A
  1. histamine: small vascular dilation, increase vascular permeability
  2. proteases: local tissue damage
  3. prostaglandins: vascular dilation
  4. leukotrienes: prolonged smooth muscle contraction
  5. cytokines: local inflammation (late-phase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

in Type I, what does primary exposure to the allergen result in?

A

activation of Th2 cells and production of IgE

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

in Type I, what does secondary exposure result in?

A

Ag-dependent cross-linking of membrane-bound IgE causing activation of mast cells –> release of inflammatory mediators

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

what are the characteristics of the immediate phase, which develops within minutes, in Type I?

A

vasodilation, congestion, edema

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

what are the characteristics of the late-phase reaction, which develops 2-24 hours later, in Type I?

A

inflammatory infiltrate, which is rich in eosinophils, neutrophils, and T cells

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

local reaction

A

asthma

inflammatory mediators from mast cells d/t allergen encounter; increase capillary permeability, spasmodic contraction of bronchs

non-immunologic stimuli includes cold and exercise

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

systemic reaction

A

anaphylaxis

d/t massive release of vasoactive amines and cytokines from mast cells – contraction of smooth m, vasodilation of capillary endothelium lowers BP and results in vascular shock while increasing difficulty of breathing

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

in Type II, which antibodies are responsible for activation of CP?

A

IgG, IgM

release of C3a and C5a during CP will result in inflammation via recruitment of leukocytes

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

in Type II, what inflammatory mediators are released from neutrophils and Mo in an Fc-dependent manner?

A

ROS, lysosomal enzymes

- will cause damage to adjacent tissues, inflammation

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

in Type II, Abs opsonize cells and lead to phagocytosis through which two receptors?

A

FcRy, CR1

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

drug-induced hemolytic anemias: drug binds directly to RBC surface, induces anti-drug Ab

A

Penicillin

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

drug-induced hemolytic anemias: auto-Ab form immune complexes w/ the drug

A

Quinidine

IC bind RBC via CR1

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

drug-induced hemolytic anemias: anti-drug Ab cross-reacts w/ Rh Ag

A

Methyldopa

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

manifestation of Type II: hemolysis, anemia

A

autoimmune hemolytic anemia

target Ag: RBC membrane pro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

manifestation of Type II: bleeding

A

autoimmune (idiopathic) thrombocytopenia purpura

target Ag: platelet membrane pro

18
Q

manifestation of Type II: nephritis, lung hemorrhage

A

Goodpasture’s syndrome

target Ag: non-collagenous pro in BM of kidney glomeruli and lung alveoli

19
Q

manifestation of Type II: hyperthyroidism

A

Grave’s disease

target Ag: TSH receptor

20
Q

manifestation of Type II: muscle weakness, paralysis

A

Myasthenia gravis

target Ag: ACH receptor

21
Q

manifestation of Type II: skein vesicles (bull)

A

pemphigus vulgaris

target Ag: pro in IC jxns of epidermal cells

22
Q

manifestation of Type II: abnormal erythropoiesis, anemia

A

pernicious anemia

target Ag: intrinsic factor of gastric parietal cells

23
Q

manifestation of Type II: myocarditis, arthritis

A

Rheumatic fever

target Ag: step cell wall Ag; Ab cross-reacts w/ myocardial Ag

24
Q

Ag-Ab IC formed in circulation and deposited in blood vessels and other tissues, including kidney and lungs

A

Type III Hypersensitivity

25
Q

which hypersensitivity results in vascular inflammation and subsequent ischemic damage to tissues d/t ICs?

A

Type III

26
Q

what is the major mechanism of tissue damage in Type III?

A

CP–recruitment of leukocytes

27
Q

manifestation of Type III: nephritis, arthritis, vasculitis

A

systemic lupus erythematosus

28
Q

manifestation of Type III: vasculitis

A

polyarteritis nodosa

29
Q

manifestation of Type III: nephritis

A

post-streptococcal glomerulonephritis

30
Q

manifestation of Type III: systemic vasculitis, nephritis, arthritis

A

serum sickness

31
Q

manifestation of Type III: cutaneous vasculitis

A

arthus reaction

32
Q

in Type III, what is injury caused by?

A

complement-mediated and Fc receptor-mediated inflammation

33
Q

the major triggers of this type are autoimmunity, exaggerated or persistent responses to environmental Ags, some microbial Ags

the only hypersensitivity mediated by cells

A

Type IV Hypersensitivity (DTH)

T-cell mediated (Th1, Th17)

34
Q

in Type IV, what cells produce cytokines causing inflammation?

A

CD4+ T (Th1, Th17), Mo, killing of host cells by CD8+ CTLs

35
Q

manifestation of Type IV: demyelination in CNS, sensory and motor dysfunction

A

MS

36
Q

manifestation of Type IV: inflammation of synovium, erosion of cartilage and bone in joints

A

RA

37
Q

manifestation of Type IV: impaired glucose metabolism, vascular disease

A

T1DM

38
Q

manifestation of Type IV: inflammation of bowel wall; abdominal pain, diarrhea, hemorrhage

A

Crohn’s

39
Q

manifestation of Type IV: DTH reaction in skin, rash

A

contact sensitivity (poison IV)

T memory cells develop after first exposure after sensitization, will evoke response 1-2 days following second exposure

40
Q

manifestation of Type IV: chronic (granulomatous inflammation)

A

chronic infections (Tb)

41
Q

cytokine-mediated inflammatory reaction in DTH, which develops 24-48 hours after Ag exposure, is primarily the result of activation of which cell?

A

CD4+ T cell

SFM Immunology (3 decks)

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