TBL 1 Flashcards

1
Q

How can antibodies specific for cell and tissue antigens cause injury?

A

They may deposit in tissues and cause injury by local inflammation, or promotion of destruction of cells, or interfere with normal cellular functions

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2
Q

How do antibodies against tissue antigens and immune complexes cause inflammation?

A

By attracting and activating leukocytes

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3
Q

What antibodies activate inflammation complexes?

A

IgG: IgG1 and IgG3

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4
Q

How do IgG1 and IgG3 cause activate inflammation complexes?

A

By binding to neutrophil and macrophage Fc receptors and activate the leukocytes

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5
Q

How is complement used in AB auto-reactivity?

A

IgG1, IgG3, IgM can activate complement (classical pathway) to cause inflammation via leukocytes

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6
Q

How can antibody deposition cause adjacent cell damage?

A

Activation of leukocytes at sites of antibody deposition these cells release ROS and lysosomal enzymes that damage adjacent tissues

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7
Q

What happens if AB bind to erythrocytes or platelets?

A

They are opsonized leading to phagocytosis

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8
Q

What are two ways AB can interfere with normal cellular functions?

A

AB stimulate receptors without the hormone present (Graves’ disease)
AB inhibit binding of neurotransmitter to receptor (Myasthenia gravis)

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9
Q

How does plasmapheresis work?

A

Reduces levels of circulating AB’s or immune complexes

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10
Q

How can B cells be targeted and depleted?

A

AB specific for CD20 can be introduced to the patient to attack B cells

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11
Q

How is T cell-dependent B cell activation inhibited?

A

AB specific for CD40L blocks the CD40L site on T cells not allowing B cells to be activated

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12
Q

How are AB used against cytokines?

A

Specific for cytokines that are necessary for B cell and plasma cell survival

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13
Q

What are two diseases that can be caused by staphylococcal infections?

A

Anti-streptococcal AB can cross-react with heart tissues in rheumatic fever
Anti-streptococcal AB can deposit in the kidney glomeruli causing post-streptococcal glomerulonephritis

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14
Q

What are three postsynaptic proteins that can be targeted in Myasthenia Gravis?

A

Nicotinic acetylcholine receptors
Muscle-specific tyrosine kinase
Low-density lipoprotein receptor-related protein 4

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15
Q

What happens when anti-AChR antibodies bind to AChR?

A

Increased endocytosis and degradation of AChR by the muscle

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16
Q

What occurs when anti-AChR bind complement factors at the post-synaptic membrane?

A

It leads to focal lysis of postsynaptic folds at the NMJ by MAC

17
Q

How do anti-AChR binding to complement factors affect AChR associated proteins?

A

Destruction of utrophin (cytoskeleton), rapsyn (anchoring site), and voltage-gated sodium channels which impairs NMJ transmission

18
Q

In mild MG what is the possible only symptom?

A

Neck muscle weakness

19
Q

General symptoms of MG?

A

Eye droopy

Expressionless face or snarl when smiling

20
Q

General clinical characteristics of LE syndrome?

A
Muscle weakness
Depressed tendon reflexes
Achy tender muscles
Dry mouth
Male impotency
Chewing, speech and swallowing difficulties
21
Q

What are general clinical biomarkers of LE syndrome?

A

Discovering malignancy

Voltage gated calcium channel AB’s

22
Q

What imaging techniques would be used for MG?

A

CT or MRI of the thorax to screen for thymomas or thymic hyperplasia

23
Q

What imaging techniques would be used for LE?

A

CT or MRI of the chest to include chest malignancy

24
Q

What is the ice pack test used for?

A

MG screening

25
Q

How is the ice pack test used?

A

Ice cube is placed over the drooping eyelid for 2 minutes and if there is improvement in ptosis, then there is a neuromuscular transmission disorder

26
Q

How to test for MG with AB?

A

Anti-AChR antibody test, if negative, run anti-Musk AB test

27
Q

How does a endrophonium test for MG work?

A

Administer endrophonium chloride which inhibits AChesterase inhibitors. It aims to demonstrate reversibility of muscle weakness

28
Q

What are the physiological roles of the thymus?

A

Main site of auto-sensitization
AChR expression by myeloid cells in thymus, in presence of inflammation it leads to the induction and maintenance of anti-AChR autoimmune responses in MG

29
Q

What is unique about people when anti-Musk ABs and anti-LRP4 AB titers are positive?

A

They do not have issues with their thymus

30
Q

Why is a thymectomy performed?

A

MG in thymamatous patients are usually more severe than in non-thymamatous patients

31
Q

How to differentiate between MG and LES?

A

Run a antibody test looking for antibodies specific for Ca antibodies