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IS FINALS AND REMOVALS > AUTOIMMUNITY > Flashcards

AUTOIMMUNITY Flashcards

1
Q

DAMAGE TO ORGANS OR
TISSUES RESULT FROM THE
PRESENCE OF THE
AUTOANTIBODY OR
AUTOREACTIVCE CELLS

A

AUTOIMMUNE DISEASE

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2
Q

SELF TOLERANCE

A
  1. Clonal deletion of relevant effector cells.
  2. Activation regulation of T cell
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3
Q

TOLERANCE MECHANISM

A
  1. Release of sequestered
    antigens
  2. Molecular mimicry
    3.Polyclonal B cell activation
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4
Q

Antigen that are protected from
encountering the circulation are not
exposed to potentially reactive
lymphocyte

A

sequestered
antigen

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5
Q

EXAMPLE OF SEQUESTERED ANTIGEN

A

Myelin Basic proteins – sequestered by BBB
Sperm – Blood-testis barrie

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6
Q

Viral or bacterial agent contain antigens
that closely resemble self antigen.
Exposure can trigger antibody production
that in turn react with similar self-antige

A

MOLECULAR MIMICRY

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7
Q

MOLECULAR MIMICRY EXAMPLE

A

Poliovirus VP2 – acetylcholine receptors
 Measles VP3 – Myelin Basic Protein (MBP)
Papilloma Virus E2 – insulin receptors

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8
Q

B CELL DEFECTS

A

B cell defects:
1. Abnormal expression or function of Regulatory signaling
molecules.
2. Dysregulation of cytokines
3. Changes in B cell development

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9
Q

the receptor for antibody that normally regulate
antibody production, may cause continual B cell stimulation.
Induce the proliferation of numerous clones of B cells
that express IgM in the absence of T helper cells. B cell can
be reactive to self antigen can be activated.

A

Defect: Fc receptor polymorphism

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10
Q

Other factors in autoimmunity

A

. Influence of hormones
2. Environmental condition
3. Defects in NK cells
4. Defects in the secretion of cytokines
5. Defects in apoptosis
6. Defects in complement componen

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11
Q

Systemic Lupus Erythematosus
(SLE)

A

Classic model of an autoimmune
disease
Systemic rheumatic disorder involving
multiple system
The immune response is directed
against the broad range of target
antigens

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12
Q

FORMS OF SLE

A
  1. Discoid (cutaneous)
     Limited to the skin and is identified by biopsy of the rash that may
    appear on the face, neck and scalp.
  2. Systemic
     More severe and can affect the skin, joints and almost all body system
     “lupus”
  3. Drug-induced
     Antiarrhythmic – procainamide hydrochloride
     Antihypertensive – Hydralazine hydrochloride
     Anticonvulsants- phenytoin
     Chlorpromazine, Isoniazid, Penicillin, sulfonamides
  4. Neonatal
     From passage of maternal autoantibodies, specifically anti-Ro/SS-A or
    anti-La/ SS-B that can affect the skin , heart and blood of the fetus and
    newborns
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13
Q

ETIOLOGY OF SLE

A

Idiopatic
1. Hormonal influences
 Estrogen
 Antiphospholipid syndrome – complication of surgery
2. Genetic predisposition
3. Environmental factor
 UV lights may cause DNA to form thymine dimers that
can result to anti DNA

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14
Q

SIGNS AND SYMPTOMS OF SLE

A

Signs and Symptoms
 Achy joints (arthralgia)
 Frequent fevers >37C
 Arthritis (swollen joints)
 Prolonged extreme fatigue
 Skin rashes
 Anemia
 Kidney involvement
 Pain in the chest on deep breathing (pleurisy)
 Butterfly-shaped rash across the cheek and nose
 Photosensitivity
 Hair loss
 Abnormal clotting problems
 Raynaud’s phenomenon
 Seizure
 Mouth and nose ulcers

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15
Q

DIAGNOSIS OF SLE

A

Diagnosis:
1. Malar rash
2. Discoid rash
3. Photosensitivity
4. Oral ulcers
5. Arthritis
6. Serositis
7. Renal disorders
8. Neurologic disorders
9. Hematologic disorders
10. Immunologic disorders
 Ab to dsDNA, SM Ag, phospholipids
11. Presence of ANA

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16
Q

Neutrophil that has engulfed the antibody-coated
nucleus of another neutrophi

A

LE cells

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17
Q

Anti ds-DNA

A

 Most specific for SLE (diagnostic)
1. Indirect Immunofluorescence (IIF)
 Crithidia luciliae
2. Immunodiffusion
3. Radioimmunoassay (RIA)
4. Enzyme immunoassay (EIA) – sensitive
-most widely used

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18
Q

Anti-histone antibody

A

Histone is a nucleoprotein that is a major
constituent of chromatin
Drug induce Lupus- w/ ss-DNA
Also found in RA and biliary cirrhosis
 Immunofluorescence assay
 Immunoblotting
EIA
 IIF- homogenous

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19
Q

DNA complexed to histone

A

Deoxynucleoprotein (DNP)

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20
Q

Anti- Sm (Smith)

A

Specific for lupus, It cannot be found in
other autoimmune
Extractable nuclear antigens represent a
family of small nuclear proteins that are
associated with uridine rich RNA
Measured by immunodiffusion,
immunoblotting, immunoprecipitation and
EIA

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21
Q

Anti SS-A/Ro and SS-B/Ro

A

Often found in cutaneous manifestations of
SLE, especially photosensitivity and
dermatitis.
Highly prevalent in scleroderma and
Sjogrens syndrome
Detected by immunoprecipitation ,
immunoblotting and EIA.

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22
Q

Anti- nRNP antibody

A

Coarsely speckled IIF pattern.
Immunoblotting, immunoprecipitation , EIA
and IIF

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23
Q

Produces prolonged activated partial
thromboplastic time (aPT) and prothrombin time
(PTT)

A

Antiphospholipid antibodies

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24
Q

Heterogenous group of antibodies that bind to
phospholipid alone or are complexed with protein.

Associated with deep-vein and arterial thrombosis
and with morbidity and pregnanc

A

Antiphospholipid antibodies

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25
Q

TREATMENT FOR SLE

A

Fever and arthritis- aspirin , antiinflammatory drug
Skin manifestation – hydroxychloroquine or
chloroquine, topical steroids
Acute fulminant lupus, lupus nephritis ,CNS
complications- systemic corticosteroids

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26
Q

Rheumatoid Arthritis

A

Strikes between 35 and 50
Characterized as chronic, symmetric and erosive
arthritis of the peripheral joints that can also affect
multiple organism such as the heart and lungs.
Can affect organs such as heart and lungs.
Associated with MHC class II which codes for beta chaiN

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27
Q

SIGNS OF RA

A
  1. Morning stiffness around the joints lasting at least 1 hour
  2. Swelling of the proximal interphalangeal,
    metacarpophalangeal, or wrist joints
  3. Symmetric arthritis
  4. Subcutaneous nodules
  5. Rheumatoid factor (RF) positive
  6. Radiographic evidence of erosions in the joints of the
    hands, wrist or both
28
Q

NON SPECIFIC SYMPTOMS OF RA

A

Non specific symptoms
 Malaise
 Fatigue
 Fever
 Weight loss
 Transient joint pain
 Nodules over bones, myocardium, pericardium, heart valves,
pleura, lungs, spleen and larynx
 Systemic: anemia,subcutaneous
nodules,pericarditris,lymphadenopathy,splenomegaly,interstiti
al lungdisease,vasculitis

29
Q

Chronic RA coupled with neutropenia, splenomegaly, and
possibly thrombocytopeni

A

Felty’syndrome

30
Q

INFECTIOUS AGENTS OF RA

A

 Mycoplasma
 Rubella
 Cytomegalovirus
 EBV
 parvovirus

31
Q

IMMUNOLOGIC FINDINGS OF RA

A

 Pannus -
 Continual inflammation
 Proinflammatory – IL1, 6, 8 ,15, 18, TNF-α
 Collagenase / tissue degrading enzymes – released from
synoviocytes and chondrocytes that line joint cavity.

32
Q

Increased cell lining of synovium and infiltration
of mononuclear cells (CD4+ lymphocytes)
-CD8+ T cells, B cells and plasma cells are scattered
- (+) Macrophage and Neutrophils

33
Q

– released from
synoviocytes and chondrocytes that line joint cavity.

A

Collagenase / tissue degrading enzymes

34
Q

AUTOANTIBODIES FOUND IN RA

A

 Rheumatoid Factor- IgM directed against the FC portion of
IgG
-Not specific
 Antikeratin antibody
 Antiperinuclear antibody
 Antifilaggrin
 Anti-Sa antibody
 Antii- CCP (Cyclic citrullinated Peptide) - lead marker for
detection of RA

 Immune complex IgG-IgM deposited in joints resulting in type
III hypersensitivity.
 C1 bind to immune complex- activate classical complement
cascade
 C3a AND C5a act as chemotactic factor- chronic -
inflammation
-
– damaged tissue

35
Q

Antibodies are against Citrullinated proteins which are
generated by modification of protein bound arginine by the
enzyme peptidylarginine deiminase

36
Q

LAB DX OF RA

A

 Clinical manifestation
 Radiographic findings
 Laboratory testing
 RF –
 Agglutination:IgM only
 Sheep RBC coated with IgG
 Latex particles – predominant because it is more sensitivity
 EIA - IgG, IgA, IgM
 Nephelometry - IgG, IgA, IgM
- scattering light of immune complex
 Anti-CCP
 EIA

37
Q

TREATMENT FOR RA

A

 Anti-inflammatory (Ibuprofen and salicylates)
 Control local swelling and pain
 Disease Modifying Antirheumatic Drugs (DMARDS)
 Methotrexate
 Hydroxychloroquine
 Sulfasalazine
 Leflunomide
 Penicillamine
 Corticosteroid (prednizone)
-halt inflammatory response
 TNF-α blocker
1. Monoclonal antibody (infliximab, adalimumab)
2.. TNF-α receptor fused to an IgG molecule
(etanercept)
Rituximab – targets CD20 antigen on B cells

38
Q

Autoimmune Thyroid Disease

A
  1. Hashimoto’s Thyroiditis
  2. Grave’s Disease
39
Q

HASHIMOTO THYROIDITIS SIGNS AND SYMPTOMS

A

 AKA Chronic Autoimmune thyroiditis
 S/S
 Goiter
 Hypothyroidism
 Dry skin
 Decreased sweating
 Puffy face with edematous eyelids
 Pallor with a yellow tinge
 Weight gain
 Dry brittle hair
 Thyroid autoantibodies

40
Q

GRAVE DISEASE S/S

A

 Hyperthyroidism`- most common cause
 Thyrotoxicosis with goiter
 Clinical symptoms
 Nervousness
 Insomnia
 Depression
 Weight loss
 Heat intolerance
 Sweating
 Rapid heartbeat
 Palpitations
 Breathlessness
 Symptoms
 Exophthalmus

41
Q

Graves disease - Antibody

A
  1. Thyroid-stimulating hormone receptor Antibody (TSHRab)
  2. Thyroid Peroxidase antibody
  3. Thyrotropin receptor-blocking antibody
42
Q

THYROID DISEASE LAB RESULTS

A

Presence of
1. Thyroglobulin antibodies - Hashimotos
 IIF – less sensitive but detect non agglutinating antibodies
- substrate: methanol fixed monkey cryostat tissue sections
 Passive Hemagglutination – tanned red blood cells
2. Thyroid peroxidase antibodies-Hashimoto’s and Grave’s
 Against enzyme that catalyzes tyrosine iodination
 EIA
 IIF
 Particle agglutination
3. TSH receptor antibodies – Grave’s disease
 Bioassay- require tissue
 Binding assay –competition between radiolabeled TSH and patient
autoimmune antibody
4. Colloid antibody (CA2)
5. TSH binding inhibitory immunoglobulin

43
Q

EGENTIC AND ENVIRONMETNAL CAUSE OF DM

A

Genetic: associated with HLA-DR3 and DR4, DQ (DQβ)
 Substitution for the amino acid 57 (Aspartic acid) of β chain
 Environmental:
 Viral infection
 Rubella virus
 Cytomegalovirus
 Coxsackie B4 virus
 Early exposure in Cow’s milk

44
Q

may act as antigen presenting cells
to activate T helper cells. Th1 then
generates TNF-α, IFN-λ and IL-1.

IN DM

45
Q

Diabetes Mellitus - Autoantibodies

A
  1. Anti-insulin antibodies
  2. Antibodies to GAD enzyme
  3. Islet cells antibodies ( ICAs)h
  4. Antibodies to
    Insulinoma antigen 2 (IA-2or ICA 512)
    IA-2βA (Phogrin)
46
Q

Diabetes Mellitus – Lab Dx

A

Islet cell Ab
 IIF – frozen section of human pancreas
RIA
Anti-insulin , Anti-GAD
RIA
EIA

47
Q

Diabetes Mellitus - Tx

A

 Insulin (IV)
 Immunosuppressive agents
 Cyclosporin A
 Azathiorpine
 Prednisone
 Anti CD-20 (Rituximab) –under research

48
Q

Multiple Sclerosis

A

Inflammatory, Autoimmune , CNS
 Formation of Plaques in the white matter of the brain and
spinal cord, leading to destruction of Myelin Sheathe of
axons
 Genetic: polymorphism in the gene coding for IL-7
 Viral:EBV,measles, Herpes simplex, Varicella, Rubella,
Influenza C, Human Herpes Virus-6, Para influenza virus

49
Q

Multiple Sclerosis- S/s

A

 Visual disturbances
 Diminished dexterity of limbs
 Locomotors incoordination
 Dizziness
 Facial palsy
 Tingling “pins and needles” of the spine or extremities
 Flashes of light seen in eye movements

50
Q

Pathogenesis OF MULTIPLE SCLEROSIS

A

Th1 (IL-1,TNF-α, INF-λ)

Th2 (IL-4,IL-5, IL-10)

Changes in endothelium to allow T cell
To penetrate BBB

Demyelination: predominant cells: T cells
and macrophage .Attachment of antibody to
myelin membrane

Acute inflammation; injury to axons and glia,
structural repair with recovery of some function
; post inflammatory neurodegeneration

51
Q

LAB RESULT OF MULTIPLE SCLEROSIS

A
  1. Oligoclonal Banding
     Increased Ig in the CSF~ CSF protein electrophoresis
     Presence of atleast 4 bands
  2. CSFprotein electrophoresis
  3. Isoelectric focusing with immunoblotting – more sensitive
  4. CSF igG index
     Compares the amount of IgG of spinal fluid to serum
     Not specific
52
Q

ANTIBODIES IN MULTIPLE SCLEROSIS

A

Antibodies against
1. Myelin basic protein peptides
2. Components of oligodendrocytes
3. Myelin membranes

53
Q

 Autoimmune disease that affects the neuromuscular junction
 Weakness and fatigability of skeletal muscle

A

Myasthenia Gravis

54
Q

S/S OF MYASTHANIA GRAVIS

A

 Early signs:
 Drooping of eyelids
 Inability to retract the corners of the mouth “snarling”
 Symptoms
 Speaking
 Chewing
 Swallowing
 Inability to support trunk, neck, head.

55
Q

Associated with presence of SLE, RA, Pernicious Anemia,
thyroiditis

A

Myasthenia Gravis

56
Q

GENETIC DEFECT IN MYASTHENIA GRAVIS

A

 Early onset (<40 yo) – HLA antigen, A1, B8 and DR3
 Late onset (>40yo) – HLA antigen B7
 Men 30-60 – DR2
 Thymic hyperplasia~ thymoma

57
Q

Myasthenia Gravis - Lab Dx

A
  1. RIA
     Blocks the binding of the receptors by anti-ACH receptor (ACHR)
     Use α-bungarotoxin snake venom to irreversibly bind to ACHR
    antibody
     Precipitation is measured
58
Q

Myasthenia Gravis - Tx

A

 Anticholinesterase agent
 Thymectomy
 Corticosteroids
 Azathioprine
 cyclosporine

59
Q

Presence of autoantibody to glomerular
basement membrane, renal tubular and
alveolar basement membrane, resulting to
renal failure and pulmonary hemorrhage
Usually occurs after viral infection

A

Goodpasteur’s Syndrome
Goodpasteur’s Syndrome

60
Q

s/s of goodpasteur syndrom

A

 Signs: Renal involvement
 Gross or microscopic hematuria
 Proteinuria
 Dec 24-hour creatinine clearance
 Inc serum BUN and Creatinine
 Signs: Pulmonary
 Hemorrhage
 Dyspnea
 Weakness
 Fatigue
 Cough

61
Q

Antibody against noncollagenous region of alpha 3 chain
type IV collagen in glomerular and alveolar basement
membranes

A

autoantibody

62
Q

Specific anti-basement antibodies

A

 Formation of smooth, linear ribbonlike pattern on direct
immunofluorescent assay of glomerular basement membrane

63
Q

lab results for goodpasteur syndrome

A
  1. RIA
  2. EIA
     Alpha 3 sub unit to detect Ab
     Less sensitive that WB
  3. IIF
     Frozen kidney sections that are incubated with patient serum and
    then overlaid with fluorescein-labelled IgG
     High false positive and negative
  4. Western blot – confirmatory
     Most sensitive and specific
64
Q

treatment for goodpasteur syndrome

A

 Plasmapheresis
 Dialysis
 Immunosuppressive drugs
 Glucocorticoids
 Cyclophosphamide
 Azathioprin

IS FINALS AND REMOVALS (5 decks)

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