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Immuno block 2 > autoimmunity > Flashcards

autoimmunity Flashcards

(55 cards)

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1
Q

What type of immune response is not present in any type of autoimmunity?

A

no IgE mediated responses

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2
Q

What is autoimmunity?

A

adaptive immunity specific for self-antigens

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3
Q

The cause of many autoimmune diseases are not known but what are the 3 main types that are known?

A

break down in the self-tolerance mechanisms of immune system

some mediated by Abs, others by T cells

some initiated by response to pathogens (molecular mimicry)

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4
Q

What are the simlarities of Type II autoimmunity and type II hypersensitivity?

A

mediated by Abs

specific for cell surface/ECM

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5
Q

What are the similarities of type III autoimmunity and type III hypersensitivity?

A

mediated by Abs

caused by immine complexes

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6
Q

What are the similarities of type IV autoimmunity and Type IV hypersensitivity?

A

mediated by T cells

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7
Q

What are mechanisms that contribute to immunological self-tolerance?

A
  • negative selection in bone marrow and thymus
  • expressionof tissue-specific proteins in thymus
  • no lymphocyte access to some tissues
  • suppression of autoimmune responses by Treg cells
  • induction of anergy in autoreactive B and T cells
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8
Q

What is autoimmune hemolytic anemia?

A

a disease that is caused by Ab (IgG or IgM) specific for surface antigens of erythrocytes

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9
Q

What can autoimmune hemolytic anemia result in?

A

activation of classical complement pathway

can result in uptake of opsonized RBC by phagocytes (in spleen) bearin either complement or Fc receptors

both result in RBC destruction

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10
Q

How would you detect autoimmune hemolytic anemia?

A

Direct Coomb’s hemagglutination assasys detect auto-Abs bound to patient’s RBCs

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11
Q

What is autoimmune (idiopathic) thrombocytopenic purpura?

A

1) IgG mediated inhibition of an enzyme responsible for cleavage of von Willdebrand factor (vWF)

vWF links platelets and blood vessels with clots

2) caused by platelet specific auto-Abs in IgG

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12
Q

What can cause autoimmune thrombocytopenic purpura?

A

caused by platelet specific auto-Abs in IgG

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13
Q

How would you diagnose a patient with autoimmune thrombocytopenic purpura?

A

observation of microangioplastic hemolytic anemia

low platelet counts

presence of schistocytes (broken RBCs)

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14
Q

How would you treat autoimmune thrombocytopenic purpura?

A

plasmapheresis (exchange transfusion) with plasma from healthy donors

rutiximab

RhoGam

steroids

splenectomy

infusion of gamma globulin

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15
Q

What is good pasture’s syndrome?

A

Ab specific for type IV collaen which lines basement membranes thru-out the body

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16
Q

In good pasture’s syndrome, what initiates the response and what are the results?

A

Ab initiates inflammatory response

kidney damage results

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17
Q

How is goodpasture’s syndrome treated?

A

plasma exchange and anti-inflammatory drugs

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18
Q

What is schleroderma?

A

inflammatory destruction of vascular endothelial cells of arterioles and smooth muscle cells

IgG mediated

many times replacement with collagen and other fibrous materials

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19
Q

Other than vascular endothelial cells what else can be affected by schleroderma?

A

kidneys, blood vessels, liver, brain

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20
Q

What are the symptoms of schleroderma?

A

localized or systemic symmetrical skin thickening

hard, smooth ivory colored areas of hardened skin

Rh factor not required for disease

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21
Q

How would you diagnose a person with schleroderma?

A

presence of anti-nuclear Abs

anti-topoisomerase Abs

anti-centromere Abs (IgGs)

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22
Q

How would you treat someone with schleroderma?

A

no known cure or standard treatment

drugs can be given to increase the blood flow to extremities

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23
Q

What causes acute rheumatic fever?

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A

caused by Abs that are produced during response to bacterial infection (group A streptococcus pyogenes)

24
Q

What is a common result of acute rheumatic fever?

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A

bacteria specific Abs cross react with heart tissue (molecular mimicry)

25
What Abs can be associated with rheumatic fever?
IgM or **IgG**
26
What are the results of acute rheumatic fever?
inflammation causes heart valve scarring and/or myocarditis
27
What is pemphigus vulgaris?
autoimmune condition mediated by IgG specific for 2 proteins this results in the loss of cohesion in keratinocytes in the epidermis
28
What are the symptoms and diagnostic tools for pemphigus vulgaris?
Sx: painful chronic blistering of skin Dx tools: punch biopsy of lesion followed by immunofleuorescent staining (IgG4 Ab considered pathogenic)
29
How would you treat pemphigus vulgaris?
corticosteroids and other anti-inflammatory drugs rituximab (CD20 specific Ab; B cell surface marker)
30
What are the autoimmune diseases the thyroid gland?
Hashimoto's throiditis Graves' disease subacute thyroiditis idiopathic hypothryoidism
31
What are the autoimmune diseeases of islets of langerhans (pancreas)?
type I diabetes type II diabetes
32
What is the autoimmune disease of the adrenal gland?
addison's disease
33
What is an antagonist wrt autoimmune disease?
molecule that binds to receptor, preventing its interaction with its specific ligand
34
What is an agonist wrt autoimmune disease?
molecule that binds to a receptor, triggering the receptor as if it is interacting with its specific ligand
35
What causes Grave's disease?
caused by Abs that bind to the thyroid stimulating hormone (TSH) receptor
36
What is the result of Graves' disease? why?
agonist=\> Ab mimics the binding of TSH to TSH receptor results in overproduction of thyroid hormone
37
What are the symptoms of Grave's disease?
* heat intolerance * nervousness * irritability * warm moist skin * weight loss * enlargement of thyroid * **bulging eye syndrome** * characteristic stare (muscle eye inflammation)
38
Would you expect the child of a pregnant woman that suffers from Goodpasture's syndrome or Grave's disease to have the disease?
yes it is IgG Abs that cause the disease and are transported into fetal circulation via the brambell receptor
39
Of the child born of the mother with the graves or goodpasture disease, would the child suffer their entire lifetime?
No once maternal Abs have been removed from fetal circulation then the child will no longer suffer symptoms of the disease possible the child willone day make an autoimmune response to the TSH receptor though
40
How is myasthenia gravis mediated? What are symptoms?
mediated by antibodies specific for actylcholine receptors on mucle cells generalized muscle weakness throughout the body especially the **face and eyelids**
41
What is the mechanism of action for myasthenia gravis? what type of antibody is it (agonist or antagonist)?
Ab binding to Ach receptors causes receptors to be endocytosed and degraded loss of receptors leaves muscles less sensitive to neuronal stimulation ANTAGONIST autoAb
42
How would you treat myasthenia gravis?
anti-inflammatory drugs alternative Tx=\> pyridostigmine =\> inhibit cholinesterase (to allow Ach to stay around longer to compete for binding)
43
What is the Ab for Subacute bacterial endocarditis? and how is it initiated?
IgG mediated inflammation of endocardium inflammation is initiated by Abs taht bind to microbes that have colonized damaged heart valves
44
typically, A patient will only develop subacute bacterial endocarditis when?
if they have already suffered damage to their heart valves
45
In subacute bacterial endocarditis, what mediated the inflammation?
phagocytes that recognize opsonized bacteria (IgG, complement opsonins) anaphylatoxins produced also promote inflammation
46
Describe mixed essential cryoglobulinemia
characterized by production of cryoglobulins
47
What are cryoglobulins?
immunoglobulins that become insoluble at reduced temperature sometimes, only light chains (Bence Jones proteins)
48
When are cryoglobulins most-often produced?
by patients that have a B cell proliferative disorder (multiple myeloma or Waldenstrom macroglobulinemia)
49
Mixed essential cryoglobulinemia is a condition that is common with what type of infection?
common sequelae to infection with hepatitis C infection
50
What mediates sytemic lupus erythematosis?
mediated by autoantibodies specific for many self macromolecules
51
What is the mechanism of action for systemic lupus erythematosis? what is the result?
* Abs bind to cell surface components * initiate inflammation * leads to tissue destruction Result=\> 1. damaged cells release soluble macromolecules 2. immune complexes form and are deposited in blood vessels, kidneys, joints (further inflammation)
52
What are some common symptoms and genetics involved in SLE?
lupus = wolf =\> characteristic facial rash most common in women (asian/African) = 1/500 severity highly variable
53
Describe the action of CD4 in the priming response for SLE
CD4 T cells specific for 1 epitope of macromolecular complex can provide help to B cells specific for other accessible epitopes of the complex
54
Describe the priming response in SLE with a B cell
A B cell that internalizes a macromolecular complex can present antigens to T cells specific for any of the proteins of the complex
55
What organ structure is generally affected with SLE?
glomerulus of kidney

Immuno block 2 (9 decks)

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