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Microbiology- Autoimmunity Flashcards

(49 cards)

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1
Q

What is autoimmunity?

A

The response of the immune system against self components

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2
Q

What % of the population is affected by autoimmune reactions?

A

5-7%

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3
Q

What populations are more affected by autoimmune reactions?

A

females and caucasians

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4
Q

What types of characteristics are definitive for autoimmune reactions?

A

autoantibodies or auto-reactive T cells specific for self-antigens

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5
Q

What type of hypersensitivity is myasthenia gravis?

A

Type II

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6
Q

Is myasthenia gravis cytotoxic or non-cytotoxic?

A

non-cytotoxic initially

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7
Q

Myasthenia gravis- epidemiology

A

females:males = 4:1

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8
Q

Which HLA molecule is involved with Myasthenia gravis?

A

HLA DR3

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9
Q

Myasthenia gravis- pathogenesis

A

autoantibodies bind to NmAchR’s –> block them –> Ach molecules can’t bind to their receptors –> flaccid paralysis

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10
Q

How does myasthenia gravis over time turn into a type II cytotoxic reaction?

A

the autoantibodies on the NmAchR’s activate complement –> inflammation –> degradation of NmAchR’s and SkM

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11
Q

Myasthenia gravis- Sx

A

muscle weakness, droopy eyelids, double vision, dyspnea

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12
Q

Myasthenia gravis- Dx

A

+ tensilon test (edrophonium)

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13
Q

How do anti-cholinesterases like pyridostigmine treat myasthenia gravis?

A

increases capacity of ACh to compete w/ autoantibodies

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14
Q

Which drug inhibits the production of autoantibodies in treatment of myasthenia gravis?

A

azathioprine

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15
Q

What type of hypersensitivity is lupus?

A

Type III

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16
Q

SLE- epidemiology

A

female:male = 15:1, 20-40 y/o, african american and asian

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17
Q

SLE- HLA involved

A

HLA DR3

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18
Q

SLE- pathogenesis

A

ciculating IgG autoantibodies specific for cells and nucleus –> binding of antibodies to cells –> inflammation –> cell/tissue destruction –> deposition of immune complexes in blood vessels, kidneys and joints –> lumpy bumpy appearance

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19
Q

SLE- Sx

A

highly variable, butterfly rash on face

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20
Q

SLE- Dx

21
Q

SLE- Tx

Study These Flashcards
A
  1. ) Immune suppression: cyclophosphamide, azathioprine, mycophenolate, leflunomide, methotrexate, belimumab.
  2. ) NSAIDS, corticosteroids
  3. ) Anti-malarial drugs
22
Q

What type of hypersensitivity is rheumatoid arthritis?

23
Q

Rheumatoid arthritis- epidemiology

Study These Flashcards
A

most common rheumatic disease, female:male 3:1, 20-40

24
Q

Rheumatoid arthritis- HLA involved

25
Rheumatoid arthritis- pathogenesis
inappropriate stimulation of B cells makes IgM Ab's specific for Fc of IgG --> rheumatoid factor made --> bind to joints --> leukocytes infiltrate the synovium --> inflammation and dmg
26
Rheumatoid arthritis- Dx
rheumatoid factor (but may not always be there and also found in SLE), elevated IgG and IgM
27
How does anti-TNF-α monoclonal antibodies (infliximab) treat rheumatoid arthritis?
eliminates cytokine, reduces inflammation as assessed by level of C-reactive protein in the blood, reduces joint swelling/pain
28
How does anti-CD20 monoclonal antibodies (rituximab) treat rheumatoid arthritis?
destroys B cells via antibody-dependent cytotoxicity
29
What type of hypersensitivity is multiple sclerosis (MS)?
type IV
30
MS- epidemiology
female:male 10:1, 20-30 y/o
31
MS- HLA involved
HLA DR2
32
MS- pathogenesis
T cells infiltrate CNS --> react with major basic protien --> demyelination of white matter --> sclerotic plaques form --> 90% of plaques contain plasma cells that secrete oligoclonal IgG in CSF
33
MS- Sx
motor weakness, impared vision, lack of coordination --> spasicity
34
MS- Dx
MRI
35
MS- Tx
1. ) IFN-β corticosteroids | 2. ) Immunosuppression
36
What happens when there is a breakdown of self-tolerance?
failure of negative selection or anergy
37
What is the role of the polyclonal B cells?
involves production of many different antibodies by many different B cells against the same antigen
38
What is the autoimmune regulator (AIRE)?
a transcription factor in the thymus that acts as an autoimmune regulator
39
What is the fxn of AIRE?
to see if T cells react with self-antigens. if they do they are identified and eliminated
40
What happens if AIRE is absent or dysfxnl?
no antigens int he thymus to help with self-reactive T cell identification/removal --> self-reactive T cells mature and enter circulation
41
What disease is caused by dysfxnl AIRE?
autoimmune polyglandular syndrome (APS)
42
What are Tregs?
a subset of CD4 T cells that have receptors specific for self antigens; they down-regulate the immune response
43
What is the mechanism of action of Tregs?
when they contact antigens presented by MHC II's, they suppress the proliferation of naive T cells responding to the self Ag that's being presented. Basically, they float around in the blood and bitch slap every T cell that reacts to self antigens. I AM THE LAW.
44
What syndrome is caused from a lack of Treg cells?
IPEX (immune dysregulation, polyendocrinopathy, enteropathy, and x-lnked syndrome)
45
What is the HLA molecule, anyway?
Human leukocyte antigen, it's the dominant genetic factor affecting sysceptibility to autoimmune disease. It's the name for the MHC in humans.
46
Which HLA causes ankylosing spondylitis and reiter's syndrome?
HLA B27
47
Why can HLA's lead to autoimmune reactions?
HLA genes have many functions, including processing of antigens and presentation of them to T-cells; obviously, if they start presenting self antigens, that would cause issues
48
Etiologies like trauma and infectious agents can do what to antigens that are normally sequestered in certain tissues?
Expose them to lymphocytes and activate them
49
What is molecular mimicry?
the resemblence of a pathogen and a host Ag

Musculoskeletal System (8 decks)

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