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Musculoskeletal System > Microbiology- Autoimmunity > Flashcards

Microbiology- Autoimmunity Flashcards

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

A

anti dsDNA

21
Q

SLE- Tx

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?

A

Type III

23
Q

Rheumatoid arthritis- epidemiology

A

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

24
Q

Rheumatoid arthritis- HLA involved

A

HLA DR4

25
Q

Rheumatoid arthritis- pathogenesis

A

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
Q

Rheumatoid arthritis- Dx

A

rheumatoid factor (but may not always be there and also found in SLE), elevated IgG and IgM

27
Q

How does anti-TNF-α monoclonal antibodies (infliximab) treat rheumatoid arthritis?

A

eliminates cytokine, reduces inflammation as assessed by level of C-reactive protein in the blood, reduces joint swelling/pain

28
Q

How does anti-CD20 monoclonal antibodies (rituximab) treat rheumatoid arthritis?

A

destroys B cells via antibody-dependent cytotoxicity

29
Q

What type of hypersensitivity is multiple sclerosis (MS)?

A

type IV

30
Q

MS- epidemiology

A

female:male 10:1, 20-30 y/o

31
Q

MS- HLA involved

A

HLA DR2

32
Q

MS- pathogenesis

A

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
Q

MS- Sx

A

motor weakness, impared vision, lack of coordination –> spasicity

34
Q

MS- Dx

A

MRI

35
Q

MS- Tx

A
  1. ) IFN-β corticosteroids

2. ) Immunosuppression

36
Q

What happens when there is a breakdown of self-tolerance?

A

failure of negative selection or anergy

37
Q

What is the role of the polyclonal B cells?

A

involves production of many different antibodies by many different B cells against the same antigen

38
Q

What is the autoimmune regulator (AIRE)?

A

a transcription factor in the thymus that acts as an autoimmune regulator

39
Q

What is the fxn of AIRE?

A

to see if T cells react with self-antigens. if they do they are identified and eliminated

40
Q

What happens if AIRE is absent or dysfxnl?

A

no antigens int he thymus to help with self-reactive T cell identification/removal –> self-reactive T cells mature and enter circulation

41
Q

What disease is caused by dysfxnl AIRE?

A

autoimmune polyglandular syndrome (APS)

42
Q

What are Tregs?

A

a subset of CD4 T cells that have receptors specific for self antigens; they down-regulate the immune response

43
Q

What is the mechanism of action of Tregs?

A

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
Q

What syndrome is caused from a lack of Treg cells?

A

IPEX (immune dysregulation, polyendocrinopathy, enteropathy, and x-lnked syndrome)

45
Q

What is the HLA molecule, anyway?

A

Human leukocyte antigen, it’s the dominant genetic factor affecting sysceptibility to autoimmune disease. It’s the name for the MHC in humans.

46
Q

Which HLA causes ankylosing spondylitis and reiter’s syndrome?

A

HLA B27

47
Q

Why can HLA’s lead to autoimmune reactions?

A

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
Q

Etiologies like trauma and infectious agents can do what to antigens that are normally sequestered in certain tissues?

A

Expose them to lymphocytes and activate them

49
Q

What is molecular mimicry?

A

the resemblence of a pathogen and a host Ag

Musculoskeletal System (8 decks)

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