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Immune and Hematological Disorders' Pathophysiology > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

¿Which of these is not a stage of Rheumatoid Arthritis?

a. Chronic established RA.
b. Preclinical RA.
c. Early and established RA.

A

a. Chronic established RA

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2
Q

Is the stage of RA that appears before clinical disease is evident, dependent to environmental factors.

a. Preclinical RA.
b. Early and established RA.

A

Preclinical RA

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3
Q

¿What is the pathological beginning of the preclinical RA?

A

Change of arginine into citrulline (citrullination) due to post translational modification.

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4
Q

¿Which of these does not cause citrullination in preclinical RA?

a. Tobacco.
b. Genetics.
c. Rheumatoid fever.
d. Infections to P. gingivalis and A. actinomycetemcomitan.

A

c. Rheumatoid fever.

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5
Q

¿Which are the main auto-ABs detected in RA?

A

ACPAS (auto-ABs against Citrillinated proteins).

RF (Rheumatoid factor against IgGs).

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6
Q

¿What are the steps of the pathogenesis in preclinical RA?

A
  1. Citrullination.
  2. MHC presentation of citrullinated proteins to TCs.
  3. TC stimulation of BCs.
  4. Production of RF and ACPAs.
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7
Q

¿What are the factors that begin the synovitis?

A
  1. ACPAs.
  2. Immune complexes (ICxs).
  3. Complement activation.
  4. microvascular insult/damage.
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8
Q

¿What is the main characteristic in “early and established RA”?

a. Synovial inflammation by CD4+ and macrophages w/ stromal activation.
b. Presence of follicular BCs in tissue.
c. Expression of IgAs against citrulline.
d. Expression of IgMs against proteins w/ citrulline.

A

a. Synovial inflammation by CD4+ and macrophages w/ stromal activation.
c. Expression of IgAs against citrulline.

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9
Q

¿Which is not a protease expressed in “early and established RA”?

a. Proteases against arginine.
b. Proteoglycans.
c. Collagenase.
d. MMPs.
e. G6Pisomerases.

A

a. Proteases against arginine.

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10
Q

True or false. In advanced stages of RA there is formation of germinal centers in the synovium.

A

True

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11
Q

What are the main tissues affected in RA?

A
  1. Synovium
  2. Primary lymphoid
  3. Mucosal tissues.
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12
Q

What is the role of fibroblasts in RA?

a. Fibrosis of the tissue.
b. Production of synovial fluid that causes edema.
c. Secretion of IL-6, MMPs, and Leukotriens.
d. Secretion of IL-1, IL-7, and TNF.

A

c. Secretion of IL-6, MMPs, and Leukotriens.

Secretion of IL-1, IL-7, and TNF is a role of MLS (macrophage-like synoviocytes).

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13
Q

What are the characteristics of pannus in RA?

A
  • presence of MLS, fibroblasts, villi, and germinal centers.
  • Angiogenesis.
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14
Q

What other immune cells can be present in the pannus and ectopic germinal centers ?

a. PMNs.
b. Eosinophils.
c. Mast cells.

A

c. Mast cells.

PMN are lacking completely.

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15
Q

What are the cells responsible for cytokine secretion that cause intimal lining expansion and activation of immune cells?

A

MLS and FLS.

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16
Q

Why is it pathological to find angiogenesis in the synovium.

a. Because it normally lacks blood supply.
b. Because it leads to PMN infiltration.
c. Because is of bad prognosis and related to angiomas.
d. Because precedes fibrosis of cartilage.

A

a. Because it normally lacks blood supply.

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17
Q

¿Where is the “window of treatment opportunity” in RA?

a. Preclinical stage.
b. Chronic Stage of RA.
c. Early and established stage.

A

c. Early and established stage.

18
Q

Which are the fibroblasts that cause the most damage?

A

Cadherin 11 positive FLS.

19
Q

What causes bone erosion of bones in RA?

a. MMPs infiltration into the trabecules.
b. Protease secretion of macrophages due to extension of the pannus.
c. RANKL expression of TCs.

A

c. RANKL expression of TCs.

Causing osteoclast activation but also by TNF, IL-1, and IL-6 from FLS.

ACPAs can react w/ citrullinated peptides of osteoclasts.

20
Q

Early ACPAs can induce the production of a cytokine in early stages of the disease, which is it ?

a. IL-5.
b. IL-10.
c. IL-8.
d. IL-22.

A

c. IL-8.

From osteoclasts, and promote PMN recruitment.

21
Q

Which are the cytokines related to JAK-STAT signaling?

A

IL-6, IFNs, IL-15, and IL-7.

STAT 1/3 involved w/ IL-6.

22
Q

What are the abnormal genes as/w RA ?

A

TP53
SENP1
PTEN

23
Q

What is the function of TNF in RA?

A

Leukocyte activation
MMP production
Angiogenesis
Arthralgias

24
Q

Which human leukocyte antigen (HLA) classes are associated with SLE?

A

HLA-DR2 and HLA-DR3

25
Q

Which are the most representative environmental triggers in SLE?

A

Cigarette smoking, UV light, drugs and estrogen

25
Q

Which complement deficiencies are the most common in SLE?

A

C1q, C2, and C4

26
Q

Type of rash characteristic in SLE

A

Malar rash, butterfly rash

27
Q

What type of rash indicates chronic skin lesion due to SLE?

A

Discoid rash

28
Q

Complication in kidneys due to SLE

A

Diffuse proliferative glomerulonephritis

29
Q

Type of hypersensitivity in SLE?

A

Type III and Type II (más III)

30
Q

What happens after a predisposed individual is triggered (SLE)?
a) deposition of immune-complexes into bloodstream
b) release of apoptotic bodies
c) formation of antinuclear antibodies
d) clearance of antinuclear antibodies

A

b

31
Q

why is SLE more common in women?

A

because estrogen is a trigger for SLE

32
Q

why do symptoms begin in SLE?

A

Because of antinuclear-antibodies deposition in tissues

33
Q

how many criteria need to be met in order to make a diagnosis?

A

4 or more

34
Q

implications of serosa damage in SLE

A

pleuritis and pericarditis

35
Q

vegetations present when SLE causes endocarditis

A

Libman-sacks (fibrin + immune cells) around mitral valve

36
Q

how many joints need to be affected to meet SLE criteria

A

2 or more joints

37
Q

antibodies found in patients with SLE

A

Antinuclear antibodies, anti-smith (targets ribonucleoproteins), anti-dsDNA, anti-phospholipid

38
Q

which antibody is seen when theres an active SLE?

A

anti-dsDNA

39
Q

which type of antibodies are more specific?

A

Anti-smith and anti-dsDNA

40
Q

medication to limit severity

A

corticosteroids and immunosuppressants

Immune and Hematological Disorders' Pathophysiology (3 decks)

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