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DIT Immunology > Imm 6 - Hypersensitivity And Complement > Flashcards

Imm 6 - Hypersensitivity And Complement Flashcards

1
Q

What is the MOA of Type I hypersensitivity?

A

Free antigen cross-links IgE bound to surface of pre-sensitized mast cell and basophils. This causes granulation of said cells, releasing histamine and bradykinin (these are vasoactive amines because they cause vasodilation and increased vascular permeability). Causes wheal and flare reaction (Hives).

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2
Q

What are the diseases/complications caused by Type I hypersensitivity?

A

Anaphylaxis. Allergic and atopic disorders (rhinitis, hay fever, eczema). Asthma.

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3
Q

What is the MOA of Type II hypersensitivity?

A

Ab against fixed antigens found on cells. There is complement-mediated damage, macrophages and NK cells that can help as well.

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4
Q

What is the test to detect Type II hypersensitivity?

A

Coombs test.

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5
Q

What are the diseases/complications caused by Type II hypersensitivity?

A

Acute hemolytic transfusion reaction. Autoimmune hemolytic anemia. Immune thrombocytopenia (ITP). Erythroblastosis fetalis. Pernicious anemia. Myasthenia gravis. Graves disease. Pemphigus vulgaris. Bullous pemphigoid. Goodpasture syndrome. Acute rheumatic fever.

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6
Q

What is the MOA of Type III hypersensitivity?

A

Antibodies against soluble antigens in the blood, forming antibody-antigen complexes deposited in tissues. This causes activation of complement and recruitment of neutrophils.

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7
Q

What are the diseases/complications caused by Type III hypersensitivity?

A

Serum sickness. Arthus reaction. SLE. Rheumatoid arthritis. Polyarthritis nodosa. Poststreptococcal glomerulonephritis.

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8
Q

What is the MOA of Type IV hypersensitivity?

A

T cell mediated. T cells bind antigen and release cytokines leading to macrophage activation and tissue damage. This is a delayed hypersensitivity and cell-mediated.

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9
Q

What are the diseases/complications caused by Type IV hypersensitivity?

A

PPD skin test. Hashimoto thyroiditis. Guillain-Barre syndrome. Multiple sclerosis. Graft-vs-host disease. Contact dermatitis.

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10
Q

What type of hypersensitivity reaction is Acute hemolytic transfusion reaction?

A

Type II.

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11
Q

What type of hypersensitivity reaction is Arthus reaction?

A

Type III.

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12
Q

What type of hypersensitivity reaction is asthma?

A

Type I.

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13
Q

What type of hypersensitivity reaction is bee sting allergy?

A

Type I.

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14
Q

What type of hypersensitivity reaction is contact dermatitis?

A

Type IV.

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15
Q

What type of hypersensitivity reaction is Acute rheumatic fever?

A

Type II.

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16
Q

What type of hypersensitivity reaction is Eczema?

A

Type I.

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17
Q

What type of hypersensitivity reaction is Grave’s disease?

A

Type II.

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18
Q

What type of hypersensitivity reaction is Guillain Barre syndrome?

A

Type IV.

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19
Q

What type of hypersensitivity reaction is GVHD (graft vs host disease)?

A

Type IV.

20
Q

What type of hypersensitivity reaction is Hashimoto thyroiditis?

A

Type IV.

21
Q

What type of hypersensitivity reaction is ITP?

A

Type II.

22
Q

What type of hypersensitivity reaction is MS (multiple sclerosis)?

A

Type IV.

23
Q

What type of hypersensitivity reaction is Myasthenia gravis?

A

Type II.

24
Q

What type of hypersensitivity reaction is PAN (polyarteritis nodosa)?

A

Type III.

25
Q

What type of hypersensitivity reaction is Type I?

A

Peanut allergy.

26
Q

What type of hypersensitivity reaction is Poststreptococcal GN?

A

Type III.

27
Q

What type of hypersensitivity reaction is RA (rheumatoid arthritis)?

A

Type III.

28
Q

What type of hypersensitivity reaction is Seasonal allergic rhinitis/

A

Type I.

29
Q

What type of hypersensitivity reaction is SLE?

A

Type III.

30
Q

What is the MOA of the Classic pathway?

A

Stimulated by antigen-Ab complexes. IgG or IgM binds antigens and then C1 complement protein. C1 is the starting point for the classic pathway: C1 inhibitor (AKA C1 esterase inhibitor) inhibits cleavage of C1 into active components.

31
Q

What is the MOA of the Alternative pathway?

A

Does not require complement. Can occur spontaneously or stimulated by molecules on surfaces of invading microbes.

32
Q

What is the MOA of Lectin pathway?

A

Mannose-binding lectin binds mannose on surface of microbe.

33
Q

What is the Membrane attack complex (MAC)?

A

The end product of complement pathway. Once assembled on site, it makes a whole in the plasma of the target cell and kill it. The proteins that come together are C5b, C6, C7, C8, C9.

34
Q

What is the job of C3b?

A

Opsonization.

35
Q

What are the two most important opsonins?

A

C3b and IgG.

36
Q

What does C3a and C5a do?

A

Anaphylaxis: C3a stimulates mast cells and basophils. C5a is involved in neutrophil chemotaxis.

37
Q

What disease has deficiency of C1 esterase inhibitor?

A

Hereditary angioedema.

38
Q

What medication should patients w/ Hereditary angioedema avoid?

A

ACE inhibitors because it increases bradykinin levels.

39
Q

What does deficiency of C3 cause?

A

Recurrent pyogenic sinus infections and respiratory tract infections (usually done by Streptococcus pneumoniae, Haemophilus influenzae). Also causes increased susceptibility to type III hypersensitivity.

40
Q

What does deficiency of C5b, C6, C7, C8, or C9 cause?

A

Increased susceptibility to Neisseria bacterimia.

41
Q

What does deficiency of DAF (decay accelerating factor) (AKA CD55) cause?

A

Keeps complements from attacking self cells in the alternative pathway. Leads to red cell lysis and Paroxysmal nocturnal hemoglobinuria.

42
Q

What is Paroxysmal nocturnal hemoglobinuria?

A

Caused by deficiency in glycosylphosphatidylinositol (GPI) which is what anchors cell surface proteins to the plasma membrane: this is essential to the anchoring of CD55 (DAF). Can also be missing CD59 (prevents membrane attacking complex to destroy cells). This leads to attack on RBCs, causing chronic intravascular hemolysis.

43
Q

What are the symptoms of Paroxysmal nocturnal hemoglobinuria?

A

Chronic intravascular hemolysis that causes Hemosiderinuria and thrombosis.

44
Q

How do we diagnose Paroxysmal nocturnal hemoglobinuria (PNH)?

A

In two ways. Ham’s test: Put RBCs in weak acid (it is positive if they lyse). Flow cytometry: Allows to look at surface markers

45
Q

What is the treatments for Paroxysmal nocturnal hemoglobinuria?

A

Transfusions. Warfarin. Eculizumab.

46
Q

A patient suffers from recurrent Neisseria infections. What complement proteins are deficient?

A

Any of the membrane attack complexes: C5b, C6, C7, C8, and C9.

47
Q

Which complement is responsible for neutrophil chemotaxis?

A

C5a.

DIT Immunology (10 decks)

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