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Pharm (Fall 2022) > Immunopharmacology (Exam V) > Flashcards

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
Q

What is Rheumatic Disease?

A
  • Rheumatoid Factor antibodies made against IgG causing progressive inflammation.
26
Q

What is an Arthus reaction?

A
  • 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
Q

What is the treatment for Type III Hypersensitivity reactions?

A
  • NSAIDs
  • Corticosteroids
28
Q

What metal can actually cause Type 4 hypersensitivity reactions?

A
  • Nickel
29
Q

What characterizes a Host vs Graft infection?

A
  • MHC-1 on the grafted organ attracts T-cells and macrophages. Host body attacks grafted organ/tissue.
30
Q

What characterizes a Graft vs Host infection?

A
  • MHC-1 on host cell is attacked by grafted tissue lymphocytes (usually bone marrow). Grafted tissue attacks all of host organs.
31
Q

What is an example of a mild Type 4 reaction?
What about a severe type 4 reaction?

A
  • Mild = poison ivy
  • Severe = Graft vs Host
32
Q

What are autoantigens?
What are autoantibodies?

A
  • Self-antigens that induce an immune response
  • Antibodies that attack autoantigens
33
Q

What are the 4 theories of autoimmunity?

A
  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
Q

What is the most common symptom of rheumatic diseases caused by autoimmunity?

A
  • Joint pain
35
Q

What characterizes the pathophysiology of SLE?

A
  • Autoantibodies attacking DNA structure.
  • Affects sites of rapid cell turnover.
36
Q

What symptom is present in 30-50% of SLE cases?
Why?

A
  • Butterfly Rash
  • Rapid cell turnover occuring on the face from sunshine exposure.
37
Q

What is the first symptom noticed with multiple sclerosis?

A
  • Muscular Weakness
38
Q

What is the pathophysiology of multiple sclerosis?

A
  • T-cell & autoantibody targeting of myelin sheath prevent normal neuron signaling.
39
Q

What is the pathophysiology of myasthenia gravis?

A
  • Autoantibodies attacking ACh receptors at the NMJ’s.
40
Q

How do glucocorticoids work?

A
  • Suppression of immune response by interfering with the cell cycle of B & T cells.
41
Q

What are the side effects of glucocorticoid use?

A
  • Immunodeficiency
  • Exogenous Cushing’s Syndrome
42
Q

What are glucocorticoids used for?

A
  • Adrenal Insufficiency (Addison’s disease)
  • Allergic & inflammatory reaction suppression
  • Asthma
  • Transplantation
43
Q

What is Calcineurin?

A
  • Protein necessary for T-cell signaling & activation.
44
Q

What two Calcineurin Inhibitors were discussed in lecture?
What were these used for?

A
  • Cyclosporine (peptide abx)- Transplants, GVHD, autoimmune disorders.
  • Tacrolimus (macrolide abx) - topical dermatitis & psoriasis
45
Q

At lower doses what is azathioprine used for?
What about at higher doses?

A
  • Immunosuppressive
  • Antineoplastic
46
Q

How does Azathioprine treat autoimmune disorders?
What is the main side effect?

A
  • Interference with purine metabolism blocks over-proliferation of cells.
  • Leukocytopenia from bone marrow suppression
47
Q

What is the metabolism pathway of Azathioprine?

A

Azathioprine → Xanthine Oxidase → 6-Mercaptopurine → 6-Thioguanine Nucleotides

48
Q

What is the primary side effect of cyclophosphamide?
What type of agent is it?

A
  • Severe Immunosuppression
  • Alkylating Agent
49
Q

What is the metabolism pathway of cyclophosphamide?

A

Cyclophosphamide → CYP450s → Acrolein & Phosphoramide Mustard (tissue toxicity & cell death)

50
Q

What is a hybridoma?

A
  • Petri dish plasma cells fused with an immortal cell line used to create monoclonal antibodies
51
Q

Which monoclonal antibody suffix is indicative of mostly human origin antibodies?

A

-umab or -zumab

52
Q

Which monoclonal antibody suffix is indicative of more chimera (human-mouse) antibodies?

A

-imab or -ximab

53
Q

What is Omalizumab?

A
  • Anti-IgE MAb used for severe asthma

Pharm (Fall 2022) (23 decks)

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