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immunology > lect 15.3 > Flashcards

lect 15.3 Flashcards

1
Q

what is the result of type 3 hypersensitivity

A

formation of antigen antibody complexes that deposit in tissues
- systemic pathogenic effects or locatlized to kidney, skin, joints

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2
Q

what is the importance of size of ag/ab complexes formed in type 3 hypersensitivity

A
  • Large complexes rapidly removed
  • small or intermediate complexes more
    pathogenic
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3
Q

what are the ags in type3

A

foreign proteins, microbial
antigens, self antigens

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4
Q

what is important in ype 3

A

integrity of mononuclear phagocytic system

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5
Q

what is the mechanism for type 3

A

activation of complement and inflammatory responses

neutrophils involved

immune complex mediated hypersensitivity

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6
Q

where are small immune xomplexes deposited when not cleared

A

in the subepithelium

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7
Q

where are large immune xomplexes deposited when not cleared

A

in the blood vessels and kidneys

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8
Q

systemic immmune complex disease

A

ags stimulate ab production and complexes formed which are noramlly cleared from circualtion but deposit in tissues inthis disease

lead to inflammatory response

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9
Q

what is the inflammatory repsone in type 3

A
  • complement activation
  • MAC formation
  • recruitment of neutrophils
  • Platelet aggregation
  • blood clots
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10
Q

what kind of disease is serum sickness

A

systemic immune complex disease identified in pre antibiotic era

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11
Q

what is the HAMA response

A

human anti mouse antibodies

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12
Q

explain how serum sickness occurs

A
  • Patients treated for infectious diseases (tetanus,
    diptheria) with horse Ab’s;
  • Ab’s to foreign Ab produced
  • Anti-horse Ab’s bind Ab and prevent further therpeutic
    benefit
  • clinical manifestations: fever, pain, skin eruptions,
    glomerulonephritis

occurs in patients treated with monoclonal antibodies made in rodents

HAMA response

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13
Q

what does the formation of circulating immune responses lead to

A
  • autoimmune diseases (SLE, RA)
  • drug reactions (penicillin, sulfonamides)
  • infectious diseases (poststreptococcal
    glomerulonephritis, meningitis, malaria)
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14
Q

goodpastures syndrome

A

type 3 and 2 hypersensitivity

  1. Production of Abs in response to viral respiratory infections
  2. Cross-reaction with normal tissue antigen in lung and kidney (molecular mimicry)

ADCC in type 2

Ig complexes in tpye 3

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15
Q

arthurs reaction

A

type 3 hypersensitivity

involves neutrophils and C3b formation of immune complexes

localized reaction

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16
Q

steps of arthurs reaction

A

PREVIOUSLY FORMED ag ab complex with igG antibodies

complement actication, thromobiss, hemmorage, acute inflammation

swelling, redness, necrosis

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17
Q

wehen does the lozalized reaction in arthurs ocur

A

4-8 hours after exposure to antigen

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18
Q

arthurs reaction responsible for reactino to

A

enviromental toxins

if patient has precipitating igG against specific protein like mold, re exposure leads to insoluble complex formation in lung tissue and

severse respiratory distress within 6-8 hours

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19
Q

what are some pulmonary typr 3 reactions

A

pigeon breeders disease

cheese washers disease

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20
Q

what is the response time of type 1 reactions

A

15-30 min

and late phase is 4-6 hours

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21
Q

what is the response time for type 2

A

mintues to hours

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22
Q

what is the response time for type 3

A

hours

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23
Q

what is cell mediated hypersensitivity

A

delayed type hypersensitivity (DTH)

24
Q

what is delayed type hypersensitivity mediated by

A

Th1 response

25
Q

what does delayed type hypersensitivity occur in response to

A

some Ags/pathogens

tuberculin reaction

26
Q

timeline for delayed type hypersensitivity

A

1st exposure- TH1 response
- sensitization phase

2nd exposure (1-2) weeks
- effector phase
-macrophage recruitment

reaction
-effector phase
-firm, red swelling

27
Q

what are some of the DTH mediating cells that occationally participate

A

TH17

TH2

CD8+

28
Q

what are the antigen presenting cells for DTH response

A

macrophages

langerhans cells

29
Q

what does the TH1 reponse in DTH in the effector phase secrete

A

cytokines- IFN Y

and chemokines

activates macrophages

30
Q

what do activateed macrophages in DTH effector phase cause

A

inc in class 2 MHC molecules

inc in TNF receptors

inc in oxygen radicals

inc in nitric oxide

31
Q

what do pateints sufferingfrom aids have a reduction of

A

CD4+ T cells

and therefore

loss of DTH

lead to deveopment of life threatening infctions that wouldnt be life threatening if it was intact DTH resopnse

32
Q

Examples of Type IV DTH Responses
TH 1-mediated

A

contact sensitivity

granulomatous hypersensititvity

tuberculin type hypersensitivity

allograft rejection

33
Q

Chemicals causing contact sensitivity are
lipid-soluble

A
  1. penetrate the skin
  2. form hapten-carrier conjugates with
    various self proteins
34
Q

what test can be used for contact sensitivity

A

patch test

solution of the suspected Ag is spread on the skin and
covered; the appearance, within 3 days, of a raised, firm, red
area indicates sensitivity

35
Q

when would we check the patch test to determine sensitivity

A

within 3 days

36
Q

what chemical indueces contact sensitivity in virtually all individuals

A

DNCB

can be used to assess patient cell mediated immunity

37
Q

what do giant cells cause

A

displacement of normal tissue

form nodules

release high concentration of lytic enzymes

destroy surrounding tissue

38
Q

what causes granulomatous hypersensitivity

A

ag no cleared

prolonged damaging DTH response

inflammatory rxn- visible granulomatous respone

activation of mcarophages which adhere to each other

fuse to for mmultinucleated giant cells

39
Q

what is the alternative of TH1 granuloma reposne

A

loprosy by mycopacterium loprae that infects macrophages in

tuberculoid form

lepromatous form

40
Q

what is the tuberculoid form of leprosy

A

cell mediated granuloma formation

destroy most bacteria

slow disease progression

better survival

41
Q

what is the lepromatous form of leprosy

A

high Ab production

depressed cell mediated immunity

many infected macrophages

extensive nerve, bone, and tissue damage

42
Q

what is the tuberculin test used for

A

evidence of exposure to DTH causing organisms

43
Q

example of tuberculin test

A

mantoux test

intraepidermal injection of purified m tuberculosis protein

44
Q

tuberculin test resutl

A

previously exposed - tuberculin like lesion at site of injection 1-2 days later

2-4 days later - full reaction

positive test indicated prior exposure

45
Q

limiation of mantoux test

A

doesnt differentiate between exposure to pathogen and vaccination

46
Q

what hypersensitivity does penicillin induce

A

any of the 4 types

47
Q

what antibody of lymphocyte is induced in type 1

A

igE

48
Q

what antibody of lymphocyte is induced in type 2

A

igM and igG

49
Q

what antibody of lymphocyte is induced in type 3

A

igG

50
Q

what antibody of lymphocyte is induced in type 4

A

Th1 cells

51
Q

how does obesity lead to chronic inflamation

A

adipose tissue secreted proinflammatory cytokines

52
Q

what are the causes of chronic inflammation

A

genetics plays a role in almost all of it

inectious and non infectous causes

obesity

53
Q

what does insulin normally signal

A

to cells that they should import glucose for the cell to prevent hyperglycemia

54
Q

what are signalling events that link obesity and inflammation to insulin resistance

A

FA bind to receptors that prevent glucose transport that was signalled by insulin

lead ot catiation of proinflammatory singnals and isnulin resistance

  • Storage of glucose as
    glycogen in the liver is
    impaired
  • Use of glucose by muscle,
    fat, B cells, brain cells, etc
    is impaired
55
Q

what receptors are involved in insulin resistance

A

TLR

IL6R

TNFR

56
Q
A

immunology (30 decks)

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