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Pharmacology > Immunopharm - inflammation and immunosuppression > Flashcards

Immunopharm - inflammation and immunosuppression Flashcards

1
Q
  1. The role of the immune system is?
  2. Innate: reactivity? affinity?
  3. Adaptive: specificity?
A
  1. Role is to distinguish “self” from “nonself” and protect the organism from nonself or infectious agents
  2. Broad reactivity, and low affinity
  3. Highly antigen-specific
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2
Q

Innate Cells:

  1. How do they defend?
  2. Secretions?
  3. Conferrence of long lasting immunity?
A

Innate Cells:

  1. Defend by neutralizing or phagocytosis
  2. Secrete cytokines/inflammatory modulators
  3. Does NOT confer long lasting immunity to the host
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3
Q

Innate Cells:

What are the 6 innate cells?

A

Innate Cells:

a. neutrophils
b. basophils
c. eosinophils
d. mast cells
e. macrophages
f. NK cells

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4
Q

Cytokines:

  1. What do cytokines bind to?
  2. What do chemokines bind to? What are the chemokines?
  3. 3 “types” of cytokines?
A

Cytokines:

  1. Cytokines bind to tyrosine kinases
  2. Chemokines bind to G-protein coupled receptors; CCL, CXCL, and XCL
  3. lymphokines (TNF, IFN), interleukins, and chemokines
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5
Q

Adaptive cells:

  1. Distinguish cells and ____ factors as self.
  2. Humoral immunity?
  3. Cellular immunity? Recognize and ___ specific pathogens
  4. Role of Helper T cells?
A

Adaptive cells:

  1. Distinguishes cells and soluble factors as self
  2. B lymphocytes: IgG, IgA, IgM, IgE, IgD
  3. T lymphocytes: Recognize and remember specific pathogens
  4. Helper T: regulate/suppress adaptive immunity
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6
Q

Function:

  1. Dendritic cell?
  2. Neutrophil?
  3. Basophil and mast cell?
A

Function:

  1. APC to stimulate T cell in lymph nodes
  2. Phagocytosis, particularly bacteria
  3. Bind IgE antibody and release histamine and other inflammatory mediators
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7
Q

Function:

  1. Tc cell? CD? MHC?
  2. Th cell? CD? MHC?
A

Function:

  1. Mediator of cellulary adaptive immunity - secretes perforins and granzymes to kill APCs; CD8; MHC-I
  2. Controls immune responses; produces cytokines that activate phagocytic cells; CD4; MHC-II
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8
Q

B lymphocyte activation:

B cell ___ antigen and digests it. Presents Ag, via ___, to ___ __ cell. The mature T cell produces cytokines for ___ of the B cell. ____ cell secretes Abs that bind matching Ags. This complex is cleaved by ___ or the spleen/___.

A

B lymphocyte activation:

B cell engulfs antigen and digests it. Presents Ag, via MHC, to mature T cell. The mature T cell produces cytokines fo the maturation of the B cell. Plasma cell secretes Abs that bind matching Ags. This complex is cleaved by compliment or the spleen/liver.

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9
Q

T lymphocyte activation:

T cells are mobilized. Encounters a ____ cell or __ cell with digested antigen with ___ display of the antigen. Cytokines from ___ and ___ cells help T cell mature. ___-Ag complex activates T cell ____ and the T cell secretes cytokines. Some cytokines induce ___ ___ cells. Some induce ____ T cells and track down cells infected with _____. Some become ___ T cells that secrete additional cytokines to ___ other immune cells.

A

T lymphocyte activation:

T cells are mobilized. Encounters a dendritic cell or B cell with digested antigen with MHC display of the antigen. Cytokines from dendritic and B cells help T cell mature. MHC-Ag complex activates T cell receptors and the T cell secretes cytokines. Some cytokines induce more T cells. Some induce cytotoxic T cells and track down cells infected with viruses. Some become helper T cells that secrete additional cytokines to attract other immune cells

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10
Q

IgA:

  1. Location?
  2. Function?
  3. Some people ____ make IgA
A

IgA:

  1. Nose/airway, GI, ears, eyes, vagina
  2. Protect body surfaces exposed to outside
  3. Some people DONT make IgA
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11
Q

IgG

  1. Location?
  2. Function?
  3. What is special about IgG?
A

IgG

  1. All body fluids
  2. Fight bacterial/viral infection
  3. IgG is the ONLY antibody that can cross placenta
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12
Q

IgM:

  1. Location?
  2. Function?
  3. Special note?
A

IgM:

  1. Blood and lymph
  2. Made in response to infection and cause other immune cells to be activated
  3. First line of defense
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13
Q

IgE:

  1. Location?
  2. Function?
A

IgE:

  1. Lung, skin, and mucous membranes
  2. Fight allergens
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14
Q

Hypersensitivity:

5 types?

A

Hypersensitivity:

a. Allergy
b. Cytotoxic, Ab-dependent
c. Immune complex
d. DTH: ab-independent and CMI
e. Autoimmune disease

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15
Q

Hypersensitivity:

  1. Allergy: examples? Ab?
  2. Cytotoxic, ab-dependent: examples? Ab?
  3. IC: examples? Ab
A

Hypersensitivity:

  1. Allergy: asthma, atopy, anaphylaxis; IgE
  2. Cytotoxic: Thrombocytopenia and autoimmune HA; IgM and IgG
  3. IC: serum sickness, RA, SLE; IgG
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16
Q

Hypersensitivity:

  1. DTH: examples? Response cells?
  2. Autoimmune: examples? Ab?
A

Hypersensitivity:

  1. DTH: contact dermatitis, MS, transplant rejection; T cells
  2. Autoimmune: graves, myasthenia gravis; IgM, IgG
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17
Q

Allergic reaction:

Initial contact with allergen causes ___ lymphocytes to produce _____. T cells interact with B cells that produce ____. Secreted ___ binds to mast cells and ____ –> ____. Later exposure to same allergen; allergen binds to ___ and activates ___ ___ and basophils. _____ –> release of histamine, cytokines, _____, leukotrienes and ______. The body response is vasodilation, ___ secretion, ____ stimulation, and smooth muscle ____.

A

Allergic reaction:

Initial contact with allergen causes T lymphocytes to produce IL-4. T cells interact with B cells that produce IgE. Secreted IgE binds to mast cells and basophils –> **sensitization**. Later exposure to same allergen; allergen binds to IgE and activates mast cells and basophils. Degranulation –> release of histamine, cytokines, interleukins, leukotrienes, and prostaglandins. The body response is vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction

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18
Q

Chronic inflammatory disease examples?

A

Peptic ulcer disease, asthma, osteoarthritis, and gout

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19
Q

Phases of the inflammatory response:

What are the 5 phases?

A

Phases of the inflammatory response:

a. vasodilation
b. plasma extravasation
c. slowing of blood flow (stasis)
d. leukocyte infiltration
e. Wound healing

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20
Q

Phases of the inflammatory response:

Leukocyte infiltration:

4 stages?

A

Phases of the inflammatory response:

Leukocyte infiltration:

a. chemoattraction
b. rolling
c. tight adhesion
d. transmigration

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21
Q

Phases of the inflammatory response:

Leukocyte infiltration:

  1. What is responsible for chemoattraction? What do endothelial cells express?
  2. What occurs in tight adhesion?
A

Phases of the inflammatory response:

Leukocyte infiltration:

  1. Macrophages release IL-1, TNF, and chemokines; endothelial cells express adhesion molecules, ICAMs, and selectins
  2. In tight adhesion, integrins are activated by PAF and bind ICAMs on endothelium
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22
Q

Mediators that cause vasodilation?

A

a. PGs (PGI/E/D)
b. NO
c. histamine

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23
Q

Mediators that increase vascular permeability?

A

a. Histamine
b. C3a and C5a
c. Bradykinin
d. LTs: LTC/D/E
e. PAF

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24
Q

Chemotaxis and leukocyte activation mediators?

A

Chemotaxis and leukocyte activation:

a. C5a
b. LTG4, LXA4, LXB4
c. Bacterial antigens

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25
Q

Tissue damage mediators?

A

Tissue damage mediators:

a. Neutrophil/macrophage lysosomal products
b. Oxygen radicals
c. NO

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26
Q

Mediators of fever?

A

Fever mediators:

a. IL-1
b. IL-6
c. TNF
d. PGE2

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27
Q

Pain/hypersensitivity mediators?

A

Mediators of pain/hypersensitivity:

a. PGE2/PGI2
b. Bradykinin
c. Tryptase
d. ATP

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28
Q

2 strategies for drugs that target the immune system?

A

2 strategies for drugs that target the immune system:

a. Attenuate signaling mediators
b. Modifying the underlying stimulus and thus removing the cause of the inflammation

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29
Q

Drug strategies for suppressing immunity/inflammation:

Drug example:

  1. Inhibition/activation of gene expression?
  2. Blockade of intracellular signalling?
  3. Costiumlation modulation?
A

Drug strategies for suppressing immunity/inflammation:

Drug example:

  1. Glucocorticoids inhibit/activate gene expression
  2. Cyclosporine/tacrolimus blocks intracellular signalling
  3. Abatacept inhibits co-stimulation of T cells
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30
Q

Drug strategies for suppressing immunity/inflammation:

Drug example:

  1. Receptor antagonism?
  2. Chemical neutralization?
  3. Blockade of synthesis?
A

Drug strategies for suppressing immunity/inflammation:

Drug example:

  1. antihistamines to block H1/montelukast and zafirlukast to block LT1 receptors - receptor antagonism
  2. Abs to TNF (infliximab) and Etanercept: pseudo receptor to TNF: chemical neutralization
  3. NSAIDs inhibit COX and Zileuton inhibits lipoxygenases: blockade of synthesis
31
Q

Drug strategies for suppressing immunity/inflammation:

Drug examples:

  1. Diminish release?
  2. Inhibit immune response?
  3. Patients on immunosuppressive meds have a 10-100x increased risk of?
A

Drug strategies for suppressing immunity/inflammation:

Drug examples:

  1. cromolyn to “stabilize” mast cells
  2. inhibit immune response: methotrexate, azathioprine, and mycophenolic acid
  3. Cancer
32
Q

Organ rejection:

  1. Hyperactute: how is it prevented?
  2. Acute: ___ response to ____ antigens.
  3. Chronic: secondary to ___ inflammation intiated by the __ cell response
  4. GVHD: ____ immune cells attack ___
  5. Which of these react to immunosuppressive therapy?
A

Organ rejection:

  1. Hyperacute: prevented with matching blood types
  2. Acute: adaptive response to donor antigens
  3. chronic: secondary to chronic inflammation initiated by the T cell response
  4. GVHD: Implanted immune cells attack host
  5. Immunosuppressive therapy is effective in Acute rejection and GVHD
33
Q

Autoimmunity:

Attack by host immune system on own tissues:

  1. Antibodies to specific antigens example?
  2. Large ag/ab complexes deposit in vessels: example?
  3. Cytotoxic T cells to tissue specific antigens: example?
A

Autoimmunity:

Attack by host immune system on own tissues:

  1. Acute rheumatic fever: ab to specific ag attack
  2. SLE: deposited complexes deposit in vessels
  3. TI diabetes: cytotoxic T cells destroy Beta cells in pancreas
34
Q

Immunosuppressants:

  1. Example of a cytotoxic drug?
  2. 2 examples of lymphotoxic drugs?
A

Immunosuppressants:

  1. Cytotoxic drug: azathioprine
  2. Lymphotoxic drugs: prednisone and ATG
35
Q

Immunosuppressants:

Drugs acting on immunocompetent cells?

A

Immunosuppressants:

Drugs acting on immunocompetent cells:

a. cyclosporine
b. tacrolimus
c. mycophenolate mofetil
d. muromonab
e. sirolimus

36
Q

Immunosuppressants:

Drugs acting on cytokines or their receptors?

A

Immunosuppressants:

Drugs acting on cytokines or their receptors:

a. Daclizumab
b. Infliximab
c. Lenalidomide
d. Etanercept
e. Thalidomide

37
Q

Azathioprine:

  1. This is a DMARD: stands for?
  2. This is a prodrug of? MOA?
A

Azathioprine:

  1. Disease-modifying antirheumatic drug
  2. Prodrug of purine analog 6-mercaptopurine; this interferes with DNA (as false nucleotide incorporation) replication and thus inhibits T and B cell proliferation
38
Q

Azathioprine:

  1. Uses?
  2. Major side effects?
A

Azathioprine:

  1. For kidney transplant and RA (off label: chrons disease, liver transplant, and GVHD)
  2. SE: Bone marrow suppression, increased suceptibility to infection, cancer, ulcer, acute pancreatitis, N/V, and anemia
39
Q

Azathioprine:

Interactions:

  1. Lower the dose when taking allopurinol: why?
  2. Use with ____ or ____ may cause leukopenia
  3. Decreases the effects of ____.
A

Azathioprine:

Interactions:

  1. Lower with allopurinol because allopurinol inhibits xanthine oxidase which is needed to break down azathoprine
  2. Use with ACE inhibitors or cotrimoxazole may cause leukopenia
  3. Decreases the effects of warfarin
40
Q

Glucocorticoids:

Name several.

A

Glucocorticoids:

hydrocortisone, cortisone, prednisone, prednisolone, methylprednisolone, dexamethasone, betamethasone, beclamethasone, fludricortisone, and aldosterone

41
Q

Glucocorticoids:

  1. Used with other immunosuppresive agents to prevent and treat?
  2. High doses of _____ for acute transplant rejection
  3. Efficacious in what 2 things? Why?
A

Glucocorticoids:

  1. Prevent and treat transplant rejection
  2. High doses of methylprednisone for acute rejection
  3. Efficacious in GVHD and autoimmune disorders (Antiinflammatory properties)
42
Q

Glucocorticoids:

4 mechanisms of action:

  1. Inhibition of _____: this is a transcription factor for?
  2. Inhibition of genes that code for what cytokines? What does this cause?
A

Glucocorticoids:

4 mechanisms of action:

  1. Inhibition of NF-kB: TF for immune mediators
  2. Inhibition of genes that code for cytokines IL1/2/3/4/5/6 as well as IL8 and TNF –> decreased T cell proliferation
43
Q

Glucocorticoids:

4 mechanisms of action:

  1. Cause __ cells to express smaller amounts of? This leads to decreased ___ synthesis and decreased amount of active ___ cells.
  2. Antiinflammatory: decreased ____ production and decreased ____ expression.
A

Glucocorticoids:

4 mechanisms of action:

  1. Cause B cells to express smaller amounts of IL-2/IL-2 receptor leading to decreased antibody synthesis and decreased amount of active _t _ cells (requires cytokines from B cells to stimulate)
  2. Anti-inflammatory: decreased ecosanoid production and decreased COX expression
44
Q

Glucocorticoids:

  1. Site of action?
  2. Metabolism?
  3. Extensive long-term use is limited by ____.
A

Glucocorticoids:

  1. Site of action: glucocorticoid response elements in DNA
  2. CYP3A
  3. Limited use bc of toxicity
45
Q

Antithymocyte Globulin (ATG)

  1. What is this?
  2. MOA: contains ___ to __ cell antigens and thus depletes?
A

Antithymocyte Globulin (ATG)

  1. Polyclonal antibodies
  2. Contains antibodies to T-cell antigens and thus depletes circulating T cells
46
Q

Antithymocyte Globulin (ATG)

Used for what 4 things?

A

Antithymocyte Globulin (ATG)

Used for:

a. induction of immunosuppression
b. acute renal rejection
c. aplastic anemia
d. prevent GVHD

47
Q

Antithymocyte Globulin (ATG)

  1. Can be used for withdrawl of ____ ____.
  2. Often used in cases where ____ resistance occurs
A

Antithymocyte Globulin (ATG)

  1. Withdrawl of calcineurin inhibitors
  2. Often used in cases where steroid resistance occurs
48
Q

Antithymocyte Globulin (ATG)

What is its most major side effect? And why?

Other SE?

Life threatening?

A

Antithymocyte Globulin (ATG)

Major: cytokine release syndrome: T cells are activated before they are destroyed and release all of their cytokines

Other: N/V, fever, HA, tremor

Life threatening: apnea, cardiac arrest, pulmonary edema (this more likely to occur with coadministration of steroids, diphenhydramine, or acetaminophen)

49
Q

Cyclosporine:

  1. What does it inhibit?
  2. Use?
A

Cyclosporine:

  1. Inhibits T cell mediated immunity
  2. For organ transplants and GVHD usually in combo with glucocorticoids and antimetabolites, also used in severe RA
50
Q

Cyclosporine:

MOA:

Cyclosporine _binds to ______ (this an immunophilin and ____ receptor in __ lymphocytes) and this inhibits production of ___ by blocking dephosphorylation of NFAT (___ ___ ___ ___) by ____, thus NFAT does not enter the nucleus

A

Cyclosporine:

MOA:

Cyclosporine binds to cyclophilin (this is an immunophilin and intracellular receptor in T lymphocytes) and this inhibits production of IL-2 by blocking dephosphorylation of NFAT (nuclear factor of activated T-cells) by calcineurin, thus NFAT does not enter the nucleus

51
Q

Cyclosporine:

  1. Metabolism?
  2. Based on the metabolism, what should not be had?
A

Cyclosporine:

  1. CYP450-3A
  2. Grapefruit juice inhibits CYP450 3A and thus should not be drank
52
Q

Cyclosporine:

Toxicity:

  1. What major toxicity occurs in the majority of patients?
  2. What occurs in 50% of renal transplant patients?
  3. Other side effects to toxicity?
A

Cyclosporine:

Toxicity:

  1. Majority: nephrotoxicity
  2. 50% renal transplant patients: hypertension
  3. Other: hirsutism, gum hyperplasia, tremor, hyperlipidemia, hepatotoxicity, and cancer
53
Q

Cyclosporine:

Drug interactions:

  1. What causes enzyme induction of hepatic metabolism?
  2. What causes enzyme inhibition in hepatic metabolism?
  3. Contraindication? Why?
A

Cyclosporine:

Drug interactions:

  1. Induction: carbamazapine and phenobarbitone (the more that the enzyme is induced: the faster the metabolism of the drug and thus more drug is needed
  2. Inhibition: antivirals (acyclovir) and antifungals
  3. Tacrolimus is contraindicated because it causes an additive effect of nephrotoxicity
54
Q

Tacrolimus:

  1. Comparison to cyclosporine? (2 differences)
  2. Metabolism?
  3. Use?
A

Tacrolimus:

  1. More potent than cyclosporine and instead of NFAT it binds to FKBP
  2. CYP450-3A (similar to cyclosporine)
  3. Used for transplantation and rescue therapy in patients with rejection episodes
55
Q

Tacrolimus:

MOA:

Inhibits __ lymphocyte activation by forming complexes with intracellular protein ____. This complex then inhibits ___ and decreases ___ production by __ cells.

A

Tacrolimus:

MOA:

Inhibits T lymphocyte activation by forming complexes with intracellular protein FKBP. This complex then inhibits calcineurin and decreases IL-2 production by T cells

56
Q

Tacrolimus:

Side effects?

A

Tacrolimus:

Nephrotoxicity and neurotoxicity (like cyclosporine)

Others: hyperglycemia, diabetes, cardiac hypertrophy, hypomagnesia, hyperkalemia

57
Q

Tacrolimus:

Drug interactions:

  1. Enzyme inducers?
  2. Enzyme inhibitors?
  3. Contraindications?
A

Tacrolimus:

Drug interactions:

  1. Inducers: anticonvulsants, rifabutin, and rifampin (bactericidal AbX)
  2. Inhibitors: antifungals
  3. NEVER give with cyclosporine (again, nephrotox)
58
Q

Sirolimus:

Structure analog of ____. Lymphocyte ____ inhibitor.

MOA:

Binds to ___ but complex does not inhibit ____, rather blocks ___ receptor signaling and arrests cell ____. This is done by blocking kinase ___ and prevents ____ mediated signal transduction to the nucleus

A

Sirolimus:

Structural analog of tacrolimus. Lymphocyte signalling inhibitor

MOA: Binds to FKBP but complex does not inhibit calcineurin, rather blocks IL-2 receptor signaling and arrests cell division. This is done by blocking kinase mTOR and prevents IL-2 mediated signal transduction to the nucleus

59
Q

Sirolimus:

  1. Use?
  2. Metabolism? Absorption? T1/2?
A

Sirolimus:

  1. Use: prophylaxis in organ transplantation
  2. CYP 3A; poor absorption; LONG T1/2
60
Q

Sirolimus:

Main side effects?

How are the side effects dissimilar to calcineurin inhibitors?

A

Sirolimus:

SE: mixed hyperlipidemia, leukopenia, thrombocytopenia, can cause lung toxicity, cancer, and anemia

Dissimilar: NOT NEPHROTOXIC and diabetes like symptoms: decreased glucose tolerance and insensitivity to insulin

61
Q

Mycophenolic Acid and Mycophenolate Mofetil:

  1. Mycophenolic acid inhibits what? Why is this important?
  2. Type of enzyme inhibition?
A

Mycophenolic Acid and Mycophenolate Mofetil:

  1. Mycophenolic acid inhibits inosine monophosphate dehydrogenase (IMPDH): this is the rate limiting step in guanosine formation for DNA –> this is important because it thus prevents proliferation of T cells, lymphocytes, and formation of antibodies from B cells. May inhibit recruitment of leukocytes to inflammatory sites
  2. non-competitive, selective, and reversible inhibition
62
Q

Mycophenolic Acid and Mycophenolate Mofetil:

  1. Difference between mycophenolate mofetil and mycophenolic acid?
  2. Why does mycophenolic acid have a preference for lymphocytes? (2 reasons)
A

Mycophenolic Acid and Mycophenolate Mofetil:

  1. MM is a produg for MA with a higher bioavailability
  2. Has a preference for lymphocytes because they depend on IMPDH for purine synthesis (because its not on the salvage pathway) and MA preferentially inhibits TII IMPDH, which is highly expressed in lymphocytes
63
Q

Mycophenolic Acid and Mycophenolate Mofetil:

  1. Uses? What can it be used with? Not used with?
  2. Major side effects?
A

Mycophenolic Acid and Mycophenolate Mofetil:

  1. For transplant rejection with glucocorticoids and calcineurin inhibitors but NOT azathioprine
  2. SE: vomitting, diarrhea, leukopenia, increased risk for infection, hypomagnesia/calcemia, hyperkalemia, anemia, increased blood sugars/cholesterol
64
Q

Mycophenolic Acid and Mycophenolate Mofetil:

Drug interactions:

  1. Enzyme inducers: antacids with _/__ hydroxides (decreases ____) and _____ (decreases enterohepatic ____)
  2. Enzyme inhibitor: ___ (antiviral: competes for tubular ____ with mycophenolic acid ____)
A

Mycophenolic Acid and Mycophenolate Mofetil:

Drug interactions:

  1. Enzyme inducers: antacids with Mg/Al hydroxides (decreases absorption) and cholestyramine (decreases enterohepatic recirculation)
  2. Enzyme inhibitor: acyclovir (antiviral: competes for tubular secretion with mycophenolic acid glucuronide)
65
Q

Muromonab-CD-3 (OKT3):

  1. What is this?
  2. Depletes available pool of?
A

Muromonab-CD-3 (OKT3):

  1. Mouse monoclonal antibody against human CD3
  2. Depletes available pool of T-cells
66
Q

Muromonab-CD-3 (OKT3):

MOA: Prevents _\_ cell activation and ______\_ by binding the receptor complex present on all _____\_ __\_ cells causing apoptosis

A

Muromonab-CD-3 (OKT3):

MOA: Prevents T cell activation and proliferation by binding the receptor complex present on all differentiated T cells causing apoptosis

67
Q

Muromonab-CD-3 (OKT3):

  1. Indications? Usually in the case of ______ resistance; not used for prophylaxis
  2. Major side effects?
  3. Potentially fatal? (3 things)
A

Muromonab-CD-3 (OKT3):

  1. Organ transplant rejection; usually in the case of glucocorticoid resistance
  2. cytokine release syndrome, infection, leukopenia, and tachyphylaxis (decreased response to the drug after administration)
  3. Potentially fatal pulmonary edema, CV collapse, and arrhythmias
68
Q

Daclizumab:

  1. What is this?
  2. Indication?
  3. Why is this good?
A

Daclizumab:

  1. Anti-CD25 mouse monoclonal antibody
  2. Given prophylactically for renal transplants
  3. Decreased incidence/severity of acute kidney rejection without increased incidence of infections
69
Q

Daclizumab:

  1. MOA: Binds to ___ receptor on activated __ cells and blocks ____ mediated ___ cell activation/___ of activated lymphocytes and ____ survival
  2. Major SE?
A

Daclizumab:

  1. MOA: Binds to IL-2 receptor on activated T cells and blocks IL-2 mediated T cell activation/expansion of activated lymphocytes and shortening survival
  2. SE: infection, anaphylactic reactions, GI, and edema
70
Q

Infliximab:

  1. What is this? Function?
  2. Uses?
  3. Adverse effects?
A

Infliximab:

  1. Monoclonal antibody against TNF-alpha; binds to TNF and neutralizes it
  2. Used in the treatment of psoriasis, Crohn’s disease, and RA
  3. Serious blood disorders, infection, lymphoma
71
Q

Etanercept:

  1. What is this? Functions as?
  2. Uses?
  3. Side effects?
A

Etanercept:

  1. TNF alpha inhibitor; binds TNF and functions as a decoy receptor
  2. Uses: RA and psoriasis
  3. SE: infection, HepB, MS, seizures
72
Q

Lenalidomide:

  1. Induces tumor cell _____. Also inhibits what?
  2. Uses?
  3. Side effects?
A

Lenalidomide:

  1. Induces tumor cell apoptosis. Also inhibits bone marrow stromal cell support
  2. Uses: multiple myeloma (blood cancer) and myelodysplastic syndromes
  3. Teratogenic, thrombosis, pulmonary embolus, hepatotoxic
73
Q

Thalidomide:

  1. Today’s medical uses?
  2. MOA?
  3. SE?
A

Thalidomide:

  1. Multiple myeloma, leprosy, and my prevent GVHD
  2. MOA: unclear
  3. teratogenic
74
Q

Rho(D) Immune Globulin:

  1. __ antibodies for ___ disease.
  2. Suppresses ___ immune system from attacking ___ blood cells which have entered the ____ blood stream from ___ circulation.
  3. Adverse effects?
A

Rho(D) Immune Globulin:

  1. IgG antibodies for Rhesus disease
  2. Suppress mother’s immune system from attacking Rh+ blood cells which have entered the mother’s blood stream from fetal circulation
  3. SE: hypersensitivity/allergic rxn, nausea, HA, dizziness, and maliase

Pharmacology (24 decks)

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