chapter 12: disorders of the immune response Flashcards

1
Q

what is hypersensitivity?

A

excessive or inappropriate activation of the immune response; damaged by immune response, NOT antigen

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

what is a hypersensitivity reaction?

A

abnormal immune response to not harmful substances –> tissue damage

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

what are the 4 types of hypersensitivity reactions?

A

1) allergic reaction
2) cytotoxic hypersensitivity
3) immune complex hypersensitivity
4) cell-mediated delayed hypersensitivity

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

what are the s/s of type 1 hypersensitivity?

A

local & atopic reactions (genetic):
1) urticaria (hives)
2) rhinitis (hay fever)
3) atopic dermatitis
4) bronchial asthma

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

what are the s/s of type 1 hypersensitivity?

A

local & atopic reactions (genetic):
1) urticaria (hives)
2) rhinitis (hay fever)
3) atopic dermatitis
4) bronchial asthma

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

what is the causative mechanism of type 1 hypersensitivity?

A

1) initial allergen exposure –> Ige antibody formation (fr B lymphocytes)
2) attach to mast cells
3) 2nd exposure –> antigen attach on mast cells –> histamine release
4) inflammatory response

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

what are the 2 types of type 1 hypersensitivity reactions?

A

1) primary/immediate phase
2) secondary/late phase

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

primary/immediate phase

A

1) mast cell degranulation releases HISTAMINE, PROSTAGLANDINS, KININS
2) vasodilation, vascular leakage, smooth muscle contraction

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

secondary/late phase

A

1) lipid mediators + cytokines release LEUKOTRIENES + PROSTAGLANDINS
2) infiltration of tissue w/eosinophils, tissue destruction

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

what is anaphylaxis?

A

a severe hypersensitive reaction (large mounts of chemical mediators released from mast cells into circulation quickly)

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

what happens as a result of anaphylactic shock?

A

1) vasodilation –> drop in BP
2) mucosa edema
3) bronchiole constriction
4) hives
5) itching
6) skin erythema
7) vomiting
8) abdominal cramping

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

what does the injection of epinephrine do?

A

1) vasoconstriction
2) increase RATE + STRENGTH of heartbeat
3) relaxes smooth bronchiole muscle

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

what are the 3 mechanisms for type 2 hypersensitivity?

A

1) complement and antibody mediated cell destruction: incompatible blood transfusion, hemolytic anemia from penicillin
2) complement and antibody mediated cell inflammation: organ rejection, tissues destroyed
3) antibody mediated cell destruction/activation: graves disease (change in cell function)

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

what is type 3 hypersensitivity?

A

free floating antigen + antibody

immune complexes deposit on bv walls and activates complement –> inflammation and bv damage

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

what are the 2 kinds of type 3 hypersensitivity?

A

1) systemic
2) local

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

what are the mechanisms of type 3 hypersensitivity?

A

1) formation of antigen-antibody complexes
2) deposition of immune complexes
3) attraction of inflammatory cells

17
Q

what is type 4 hypersensitivity?

A

cell mediated: sensitized t cells attack antigen

18
Q

what are the 2 types of type 4 hypersensitivity?

A

1) direct cell-mediated cytotoxicity
2) delayed-type hypersensitivity

19
Q

what is the difference between delayed cell-mediated cytotoxicity and delayed-type hypersensitivity?

A

cmc: ctc directly kill antigen containing cell
dth: response to soluble protein antigen (poison ivy)

20
Q

allograft

A

same species

21
Q

isograft

A

identical twins

22
Q

autograft

A

one part of body to another

23
Q

xenograft

A

between different species

24
Q

hyperacute rejection

A

patient has antibodies against transplant in them IMMEDIATELY

25
Q

acute rejection

A

SEVERAL WEEKS AFTER; unmatched antigens cause a reaction

26
Q

chronic/late rejection

A

SEVERAL MONTHS AFTER; bv’s in graft are gradually damaged

27
Q

graft vs host disease

A

when donated stem cells or bone marrow wbc attack host body

28
Q

the perfect storm

A

1) transplant must have a functional cellular immune component
2) recipient tissue: antigens foreign to donor t-lymphocytes
3) recipient tissue: compromised where it can’t destroy transplanted t cells

29
Q

how do we prevent rejection of a transplant?

A

1) match hla/mhc
2) use of immunosuppressant drugs

30
Q

autoimmune disease

A

self-tolerance breaks down
immune system attacks self-antigens –> destroys body tissues

31
Q

immunodeficiency

A

loss of part or all function of immune system; acute or chronic

32
Q

what are the two kinds of immunodeficiency?

A

1) primary: genetic, congenital disorders
2) secondary/aquired: malnutrition, drug induced, caused by infection (hiv)

33
Q

what are some effects of immunodeficiency?

A

1) opportunistic infections
2) arise from normal flora
3) difficult to treat
4) increased risk of cancer

34
Q

treatments of immunodeficiency disorders

A

1) antibody replacement
2) bone marrow/thymus replacement

35
Q

hiv

A

human immunodeficiency virus: transmitted by body fluids (sexual contact, breast milk, blood-to-blood contact)

36
Q

phases of hiv

A

1) primary infection: s of systemic infection are flu-like, antibodies against hiv appear (1-6 mo)
2) latency phase: virus replication, t helper cell count falls
3) overt aids: t helper cell count <200 cells

37
Q

associated illnesses of aids

A

1) opportunistic infections (respiratory, gastrointestinal, nervous)
2) malignancies: kaposi sarcoma, non-hodgkins
3) wasting syndrome
4) metabolic disorders