Immunopharmacology (Exam V) Flashcards

1
Q

How many lines of defense does the body have?
Which of these are innate/nonspecific?

A
  • 3
  • First & second line of defense are innate/nonspecific.
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2
Q

What characterizes the body’s first line of defense?

A
  • Physical barriers like skin.
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3
Q

What characterizes the body’s second line of defense?

A
  • Phagocytosis
  • Inflammation
  • Fever
  • Antimicrobial proteins
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4
Q

What characterizes the body’s third line of defense?

A
  • B cells & T cells
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5
Q

What is acquired natural passive immunity?
How long does it last?

A
  • IgE antibodies from maternity.
  • 6-9 months
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6
Q

What is an example of acquired natural artificial immunity?

A
  • Antivenom for snake bites
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7
Q

Where are B-cells developed?
Where are T-cells developed?

A
  • Bone marrow
  • Thymus
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8
Q

What do B cells do after interacting with an antigen?

A
  • Turn into plasma cells (Ab producers)
  • Turn into long-lived memory cells
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9
Q

What is opsonization?

A
  • The coating of an antigen
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10
Q

MHC 1 is associated with what T-cell type?
MHC 2 is associated with what T-cell type?

A
  • CD8 Killer cells
  • CD4 helper cells
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11
Q

What cells are characterized by cell-mediated immunity?
What cells are characterized by humoral immunity?

A
  • T-cells
  • B-cells (Ab immunity)
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12
Q

What type of antibody is specific for a singular pathogen?

A

IgG

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13
Q

Is primary or secondary immunodeficiency genetic?

A
  • Primary immunodeficiency
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14
Q

What characterizes Type I hypersensitivities?

A
  • Mild or severe anaphylaxis (hay fever, food allergies, etc.)
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15
Q

What characterizes Type II hypersensitivities?

A
  • Antibody-mediated hypersensitivities (Blood incompatibilities)
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16
Q

What characterizes Type III hypersensitivities?

A
  • Immune Complex hypersensitivities (Rheumatoid arthritis)
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17
Q

What characterizes Type IV hypersensitivities?
What is unique about this class of hypersensitivities?

A
  • Cell-mediated Delayed hypersensitivities (poison ivy example)
  • No Ab involvement, just T-cells.
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18
Q

What are some examples of primary immunodeficiency?

A
  • DiGeorge Syndrome (No thymus = no t-cells)
  • Agammaglobinemia (no B-cells = no Ab’s)
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19
Q

What is an example of secondary (acquired) immunodeficiency?

A
  • AIDS
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20
Q

What two scenarios for Type II Hypersensitivity reactions were discussed in lecture?

A
  • Transfusion reaction
  • Hemolytic disease of the newborn.
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21
Q

What is the pathophysiology of Newborn Hemolytic Disease?
What is the treatment?

A
  • Rh⁺ fetus in an Rh⁻ mother (firstborn) → (secondborn) IgG from first pregnancy attacks newborns RBCs.
  • RhoGAM
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22
Q

What is the hallmark sign of Type III Hypersensitivity reactions?

A
  • Joint Pain
23
Q

What does Rheumatic mean?

A
  • Joint Cavity
24
Q

What is the general pathophysiology of Type III Hypersensitivity reactions?

A
  • Deposition of immune complexes in joints where WBCs migrate to and cause inflammation.
25
What is Rheumatic Disease?
- Rheumatoid Factor antibodies made against IgG causing progressive inflammation.
26
What is an Arthus reaction?
- Acute response to multiple vaccine injections at the same site causing immune complex formation in the subcutaneous tissue. Results in localized redness, hemorrhage, & eventual necrosis
27
What is the treatment for Type III Hypersensitivity reactions?
- NSAIDs - Corticosteroids
28
What metal can actually cause Type 4 hypersensitivity reactions?
- Nickel
29
What characterizes a Host vs Graft infection?
- MHC-1 on the grafted organ attracts T-cells and macrophages. **Host body attacks grafted organ/tissue**.
30
What characterizes a Graft vs Host infection?
- MHC-1 on host cell is attacked by grafted tissue lymphocytes (usually bone marrow). **Grafted tissue attacks all of host organs**.
31
What is an example of a mild Type 4 reaction? What about a severe type 4 reaction?
- Mild = poison ivy - Severe = Graft vs Host
32
What are autoantigens? What are autoantibodies?
- Self-antigens that induce an immune response - Antibodies that attack autoantigens
33
What are the 4 theories of autoimmunity?
1. Exposure to antigens previously sequestered from the immune system. 2. Molecular mimicry - pathogen similar to host tissue (streptococcus pyogenes attacking heart valves causing rheumatic fever) 3. Inappropriate expression of MHC II on cells that don't normally express it (islet β cells = DM) 4. Hygiene hypothesis
34
What is the most common symptom of rheumatic diseases caused by autoimmunity?
- Joint pain
35
What characterizes the pathophysiology of SLE?
- Autoantibodies attacking DNA structure. - Affects sites of rapid cell turnover.
36
What symptom is present in 30-50% of SLE cases? Why?
- Butterfly Rash - Rapid cell turnover occuring on the face from sunshine exposure.
37
What is the first symptom noticed with multiple sclerosis?
- Muscular Weakness
38
What is the pathophysiology of multiple sclerosis?
- T-cell & autoantibody targeting of myelin sheath prevent normal neuron signaling.
39
What is the pathophysiology of myasthenia gravis?
- Autoantibodies attacking ACh receptors at the NMJ's.
40
How do glucocorticoids work?
- Suppression of immune response by interfering with the cell cycle of B & T cells.
41
What are the side effects of glucocorticoid use?
- Immunodeficiency - Exogenous Cushing's Syndrome
42
What are glucocorticoids used for?
- Adrenal Insufficiency (Addison's disease) - Allergic & inflammatory reaction suppression - Asthma - Transplantation
43
What is Calcineurin?
- Protein necessary for T-cell signaling & activation.
44
What two Calcineurin Inhibitors were discussed in lecture? What were these used for?
- Cyclosporine (peptide abx)- Transplants, GVHD, autoimmune disorders. - Tacrolimus (macrolide abx) - topical dermatitis & psoriasis
45
At lower doses what is azathioprine used for? What about at higher doses?
- Immunosuppressive - Antineoplastic
46
How does Azathioprine treat autoimmune disorders? What is the main side effect?
- Interference with purine metabolism blocks over-proliferation of cells. - Leukocytopenia from bone marrow suppression
47
What is the metabolism pathway of Azathioprine?
Azathioprine → *Xanthine Oxidase* → 6-Mercaptopurine → 6-Thioguanine Nucleotides
48
What is the primary side effect of cyclophosphamide? What type of agent is it?
- Severe Immunosuppression - Alkylating Agent
49
What is the metabolism pathway of cyclophosphamide?
Cyclophosphamide → *CYP450s* → Acrolein & Phosphoramide Mustard (tissue toxicity & cell death)
50
What is a hybridoma?
- Petri dish plasma cells fused with an immortal cell line used to create monoclonal antibodies
51
Which monoclonal antibody suffix is indicative of mostly human origin antibodies?
-umab or -zumab
52
Which monoclonal antibody suffix is indicative of more chimera (human-mouse) antibodies?
-imab or -ximab
53
What is Omalizumab?
- Anti-IgE MAb used for severe asthma