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MFMII > Type II and III Hypersensitivity Reactions > Flashcards

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
Q

what does deposition of the complexes cause?

A
  1. activation of complement
  2. release of anaphylotoxins from complement pathways (c3a, c5a)
  3. inflammatory damage to the tissues
26
Q

normal body response to immune complexes

A

PMN and macrophages bind to immune complexes via FcR (IgG) and phagocytize the complexes

27
Q

abnormal body response to immune complexes

A

unable to phagocytize, so immune complexes cause inflammation via complement activation and frustrated phagocytes

28
Q

what are frustrated phagocytes

A

cells that cannot phagocytize an immune complex degranulate in the area of immune complex deposition and trigger chronic inflammation

29
Q

what occurs if IC deposits in the joints?

A

arthritis

30
Q

what occurs if IC deposits in the kidneys?

A

glomerulonephritis, lupus

31
Q

what is serum sickness

A

when infectious disease is treated with antisera against bacterial toxins like diphtheria, tetanus, botulinum

32
Q

describe the classic manifestation of serum sickness

A
  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
Q

what is SSLR

A

serum sickness like reaction from use of Monoclonal antibodies produced in rodents

34
Q

what causes rheumatic fever?

A

sequelae from strep A infection, cross reactivity of GAS Ab with heart muscle tissue and the glomerular basement membrane occurs.

35
Q

symptoms of rheumatic fever?

A

hx of GAS infection, diffuse joint and body pain, swelling of hands and feet, erythematous rash on lower extremities

36
Q

treatment of rheumatic fever

A

treat GAS!

37
Q

what causes rheumatoid arthritis

A

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
Q

treatment for RA

A

corticosteroids, NSAID, disease modifying antirheumatic drugs (DMARD)

39
Q

what is systemic lupus erythmatosus (SLE)

A

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
Q

symptoms of SLE

A

malar (butterfly) rash, fatigue, wt loss, arthritis of hands., decreased Hb, presence of antinuclear Ab

41
Q

gender differences in SLE

A

more common in women, more aggressive in men

42
Q

symptoms of glomerulonephritis

A

puffiness of face upon waking, urine with trace blood, decreased urination, coughing, SOB, HBP, can cause complete kidney failure

43
Q

treatment of glomerulonephritis

A

decrease protein, salt, K intake
diuretics to treat puffiness and swelling
take Ca supplements

MFMII (29 decks)

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