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MNI (immuno path) > L26- Autoimmune Diseases > Flashcards

L26- Autoimmune Diseases Flashcards

1
Q

Autoimmune disease previous names

A

CT diseases

collagen vascular disease

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2
Q

describe central tolerance process

A

(T cells in thymus and B cells in BM)

1) APC presents self Ag in thymus or BM
2) immature T/B cell binds with high, low, or no affinity

3a, thymus) high affinity, T cell deletion or Treg cell; low affinity, reprogramming

3b, BM) high affinity, B cell deletion; low affinity, reprogramming

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3
Q

describe peripheral tolerance process

A
  • backup mechanism to neutralize self-reactive T and B cells (if they escape central neutralization)
    1) APC presents self in periphery – T cell or B cell binds

2a) suppression of T cell via Treg cells
2b) T cell deletion
2c) T cell anergy- failure of response

2d) B cell anergy- failure to respond

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4
Q

Autoimmune mechanisms in general involve the following 3 processes before occurring

A

1) Loss of Self-Tolerance via genetic predisposition – multifactorial, due to multiple and many mutations = ‘susceptibility genes’
2) tissue injury or 3) infection –> change to self-Ag

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5
Q

______ is the common genetic locus with relation to Autoimmune diseases (bonus- specific gene for ankylosing spondylitis)

A

HLA locus

HLA-B27 for ankylosing spondylitis (strong association – weaker for other autoimmune diseases)

-note many other loci can be involved

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6
Q

briefly describe the ways infections and injury contribute to the Autoimmune mechanism

A
  • Molecular mimcry (infection): microbes with cross-reactive epitopes with self-Ags
  • Up-regulation of immune response (more sensitive and hyperactive) due to inflammation and necrosis (trigger)
  • altered display of self-Ag
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7
Q

SLE:

  • affects (males/females) more
  • (2) and (3) contribute to etiology
  • (4) are the affected systems
  • (5) is common in terms of associated diseases
A

1- females, 9:1

2- genetic susceptibility
3- environmental triggers (proposed mechanism has triggers damaging tissue, releasing many DNA Ags)

4- skin, kidneys, serosa, joints, heart

5- overlaps with other autoimmune diseases

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8
Q

SLE involves (1) as the basic mechanism with (2) as the predominant antibodies. SLE is a type (3) hypersensitivity reaction.

A

1- loss of self-tolerance

2- Abs against nuclear components (Anti-dna), Abs against phospholipids/others

3- type II (Ig targets membrane Ag, direct Ab injury), type III (immune complex deposition)

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9
Q

SLE, skin effects:

  • (1) is most common, worsened by (2)
  • (3) may be present
A

1- malar / butterfly rash — non-scarring

2- sun light (photosensitive)

3- features of vasculitis

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10
Q

describe microscopic appearance of SLE in the skin

A
  • inflammatory cell infiltration
  • edematous tissue around vacuolar/liquefactive necrosis via basal keratinocyte degeneration

-IgG present on immunofluorescence on stratum basale layer of epidermis (basal keratinocytes) due to abundance of nuclear products (in comparison to surrounding cells)

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11
Q

list the different presentations of SLE in the kidney (hint: I-V)

A

I- normal LM, deposits on IF

II- (10-20%) mesangioproliferative glomerulonephritis

III- (20-35%) focal proliferative glomerulonephritis

IV- (35-60%) diffuse proliferative glomerulonephritis

V- (10-15%) membranous glomerulonephritis

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12
Q

describe the effects SLE has on joints

A
  • pain, swelling, inflammation, stiffness of joints
  • neutrophils and fibrin in synovial fluid
  • non-erosive synovitis == articular cartilage intact
  • no deformities
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13
Q

describe the effects SLE has on Heart + BVs

A

Heart:

  • pericarditis, myocarditis
  • Libman Sacks endocarditis: 1-3 mm aseptic vegetation on any valve on either surface

BVs:
-necrotizing vasculitis of small arteries, arterioles (via complement activation) –> effects any tissue –> complete CNS angiograph

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14
Q

SLE Diagnosis (Igs):

  • (1) testing is specific and diagnostic
  • (2) testing is useful because it is sensitive, but nonspecific
  • (3) are the ‘other’ antibodies that can be tested
A

1- anti-dsDNA, anti-Smith

2- ANA, anti-nuclear antibodies via indirect IF

3- *anti-phospholipid, anti-platelet, anti-RBC

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15
Q

list the many other tests that are useful in diagnosis and monitoring of SLE (indicate what each is checking for)

A
  • UA and renal function tests: kidney status
  • kidney biopsy if necessary
  • CBC: hemolysis
  • coagulation studies: platelet destruction
  • complement levels: reduced in active disease b/c of deposition
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16
Q

describe the SLE diagnostic criteria according to ACR

A

4 out of 11 of the following:

  • malar (cheek) skin rash
  • discoid (disc shaped) skin rash
  • photosensitive rash
  • oral ulcers
  • arthritis
  • serositis
  • renal / neurologic / hematologic / immunologic disorder
  • anti-nuclear Ab (ANA)
17
Q

Anti-phospholipid Abs are found in (1)% of SLE patients. (2) is the main change as a result, which can lead to (3) or (4).

A

1- 40-50%

2- prolongs coagulation time (in vitro)

3- recurrent thromboemboli (in vivo)
4- recurrent abortions, focal cerebral ischemia (in vivo)

18
Q

define anti-phospholipid antibody syndrome

A

presence of anti-phospholipid Ab w/o criteria to meet SLE Dx (presents alone)

19
Q

Drug-induced SLE:

  • (1) list drugs, indicate most common cause
  • (2) are frequently measured / present
  • (3) Sxs are commonly not present
  • (4) doesn’t occur with drug removal
A

1- procainamide* (most common), hydralazine, isoniazid, D-penicillamine

2- anti-histone Abs

3- renal and CNS (no encephalopathy)

4- improvement of Sxs or eradication of SLE

20
Q

Systemic Sclerosis = (1):

  • (2) definition
  • (3) are the affected systems
  • (4) are the systemic types
A

1- scleroderma

2- excessive fibrosis throughout body

3:

  • skin (100%), GIT (90%), lungs (50%)
  • kidneys, heart, skeletal muscle (less common)

4- diffuse or limited (= CREST syndrome)

21
Q

Systemic Sclerosis:

  • (1) affected age range
  • affects (males/females) more
  • overlapping features with (3) and (4), where their features may be masked
A

1- 50-60 y/o
2- females (3:1)

3- SLE
4- RA

22
Q

describe skin features of Systemic Sclerosis

A
  • skin sclerosis –> fingers affected first –> UEs, neck, face
  • Reynaud’s phenomenon: reversible vasospasm with white/ischemic, blue/cyanotic, red/hyperemic areas

-fibrosis and atrophy of muscles – limited ROM, ulcers

23
Q

describe GIT features in scleroderma

A
  • muscular atrophy and fibrosis –> strictures in GIT (vomiting) or esophagus (dysphagia)
  • loss of normal motility and absorption
24
Q

It is thought that (1) are the main mediators of scleroderma, explain.

  • (2) is highly specific humoral abnormality (although non-pathogenic)
  • (3) is highly specfic for CREST syndrome
A

1- fibroblastic activation via CKs from Th cells –> macrophages and mast cells –> fibrogenic CKs –> sclerosis

2- Anti-topoisomerase (anti-Scl 70)
3- Anti-centromere

25
Q

list the two main microscopic features of scleroderma in the skin

A
  • flattening of epidermis (less troughs and pits)

- focal lesion of inflammatory cells

26
Q

describe the differences in development and presentation of CREST in comparison to diffuse systemic sclerosis

A

-limited form – mild and indolent course

Sxs: CREST
Calcinosis (Ca deposition in soft tissues)
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly (skin thickening => hypomobility, ulceration)
Telangestasia (spider veins)

27
Q

Graves disease = (1):

  • (2) affected age range
  • affects (males/females) more
A

1- diffuse toxic hyperplasia of thyroid

2- 20s-30s

3- females

28
Q

______ are the Abs for Graves disease

A
  • TRS-Ab, thyrotropin-receptor stimulating Ab
  • TPO-Ab, thyroid peroxidase Ab
  • TBII-An, thyrotropin binding inhibitor Ig
29
Q

list symptoms of Graves disease

A 
(hyperthyroidism)
heat intolerance
increased appetite, weight loss
palpitations -- AFib
tremor
myopathy
ophthalmopathy (exophthalmos)
30
Q

Autoimmune Gastritis = (1):

  • Abs against (2)
  • (3) decrease leads to (4)
  • (5) decrease leads to (6)
A

1- atrophic gastritis of pernicious anemia
2- gastric parietal cells

3- dec acid secretion
4- poor digestion / absorption

5- Intrinsic Factor
6- B12 deficiency –> macrocytic anemia + neurological symptoms

MNI (immuno path) (14 decks)

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