Type II and III Hypersensitivity Reactions Flashcards

1
Q

how is type II reaction stimulated?

A

binding of Ab to cell surface Ag, initiating cytotoxicity

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2
Q

how is type III reaction stimulated

A

soluble Ag-Ab complexes deposited in tissues

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3
Q

what is ABO incompatibility?

A

Ab against RBC antigen binds and mediates killing via complement or ADCC (type II)

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4
Q

what does blood transfusion reaction cause?

A

systemic inflammation and RBC lysis

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5
Q

what is erythtroblastosis fetalis?

A

a hemolytic disease of a newborn, where a Rh+ is born to a Rh- mother, the 1st baby is fine but the 2nd time, mother has Ab against Rh from 1st pregnancy. the anti Rh-Ab or cells cross placenta and maternal Ab attach fetal RBC

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6
Q

how to treat erythroblastosis fetalis?

A

treat mother with Ab to Rh (RhoGAM) right after 1st birth

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7
Q

what is autoimmune hemolytic anemia?

A

autoantibodies attach RBC that are carrying foreign substances (like drug metabolites, microbial Ag), and immune system just sees the Ab bound to “foreign Ag” on a cell, stimulates ADCC.

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8
Q

early sx autoimmune hemolytic anemia?

A

SOB and pale skin

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9
Q

what could cause autoimmune hemolytic anemia?

A
  1. mycoplasma pneumonia infection

2. drug reactions to ACE inhibitors or sulfa-trimethoprim

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10
Q

how does mycoplasma pneumonia cause autoimmune hemolytic anemia?

A

induces Ab that cross react with RBC antigens (classic hemolytic anemia)

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11
Q

how do drug reactions causes autoimmune hemolytic anemia

A

drug binds to RBC surface and Ab against the drug binds and causes RBC lysis

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12
Q

what is goodpasture’s nephritis?

A

anti-glomerular basement membrane disease (anti-GBM disease) that causes severe illness

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13
Q

what happens in goodpasture nephritis?

A

Ab bind to basement membranes of the kidneys and lungs and activate complement

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14
Q

how to diagnose anti-GBM?

A

blood in urine, foamy urine, swelling in legs, HBP

urinalysis, blood test, CXR, kidney Bx

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15
Q

treatment of anti-GBM?

A

oral immunosuppressive drugs like cyclophosphamide and corticosteroids

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16
Q

cause of myasthenia gravis?

A

production of auto-Ab to acetyl choline receptor (AchR) that causes weakness of muscles responsible for breathing and moving face, eyes, arms, legs.

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17
Q

diagnose MG?

A

ptosis, weakness, blood test looking for auto-Ab

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18
Q

treatment for MG

A

acetylcholinesterase inhibitor (donepezil), immunosuppressive therapies, immunomodulary (IVIG)

19
Q

massive infiltration of what cell type occurs during Type III?

A

neutrophils

20
Q

what is the localized effect of type III reactions?

A

arthus reaction that causes vasculitis

21
Q

what is vasculitis

A

rupture of blood vessels and hemorrhage

22
Q

what is a cause of vasculitis?

A

injections of Ig against diptheria and tetanus toxins, or immunizations of humans with animal serum (gets worse with each inoculation)

23
Q

what is the systemic effect of type III reactions?

A

immune complex deposition

24
Q

what triggers immune complex formation?

A

any kind of Ag can be the trigger

25
what does deposition of the complexes cause?
1. activation of complement 2. release of anaphylotoxins from complement pathways (c3a, c5a) 3. inflammatory damage to the tissues
26
normal body response to immune complexes
PMN and macrophages bind to immune complexes via FcR (IgG) and phagocytize the complexes
27
abnormal body response to immune complexes
unable to phagocytize, so immune complexes cause inflammation via complement activation and frustrated phagocytes
28
what are frustrated phagocytes
cells that cannot phagocytize an immune complex degranulate in the area of immune complex deposition and trigger chronic inflammation
29
what occurs if IC deposits in the joints?
arthritis
30
what occurs if IC deposits in the kidneys?
glomerulonephritis, lupus
31
what is serum sickness
when infectious disease is treated with antisera against bacterial toxins like diphtheria, tetanus, botulinum
32
describe the classic manifestation of serum sickness
1. antiserum from animals is injected into humans 2. Ab against animal serum produced 3. fever, arthralgia, lymphadenopathy, rashes/hives seen within hours 4. rupture of BV and hemorrhage
33
what is SSLR
serum sickness like reaction from use of Monoclonal antibodies produced in rodents
34
what causes rheumatic fever?
sequelae from strep A infection, cross reactivity of GAS Ab with heart muscle tissue and the glomerular basement membrane occurs.
35
symptoms of rheumatic fever?
hx of GAS infection, diffuse joint and body pain, swelling of hands and feet, erythematous rash on lower extremities
36
treatment of rheumatic fever
treat GAS!
37
what causes rheumatoid arthritis
autoantibodies specific for IgG and IgM (anti-Ig autoAb) bind to Fc region of normal IgG in the synovial membranes of joints. this activates complement, attracts neutrophils, and causes inflammation
38
treatment for RA
corticosteroids, NSAID, disease modifying antirheumatic drugs (DMARD)
39
what is systemic lupus erythmatosus (SLE)
chronic inflammatory autoimmune response that causes chronic activation of lymphocytes. activation of complement produces C5a, which attracts neutrophils and releases enzymes, causes systemic damage.
40
symptoms of SLE
malar (butterfly) rash, fatigue, wt loss, arthritis of hands., decreased Hb, presence of antinuclear Ab
41
gender differences in SLE
more common in women, more aggressive in men
42
symptoms of glomerulonephritis
puffiness of face upon waking, urine with trace blood, decreased urination, coughing, SOB, HBP, can cause complete kidney failure
43
treatment of glomerulonephritis
decrease protein, salt, K intake diuretics to treat puffiness and swelling take Ca supplements