Immunopharm - inflammation and immunosuppression

Question 1

1. The role of the immune system is?
2. Innate: reactivity? affinity?
3. Adaptive: specificity?

Answer 1

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

Question 2

Innate Cells:

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

Answer 2

Innate Cells:

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

Question 3

Innate Cells:

What are the 6 innate cells?

Answer 3

Innate Cells:

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

Question 4

Cytokines:

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

Answer 4

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

Question 5

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?

Answer 5

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

Question 6

Function:

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

Answer 6

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

Question 7

Function:

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

Answer 7

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

Question 8

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/___.

Answer 8

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.

Question 9

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.

Answer 9

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

Question 10

IgA:

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

Answer 10

IgA:

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

Question 11

IgG

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

Answer 11

IgG

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

Question 12

IgM:

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

Answer 12

IgM:

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

Question 13

IgE:

1. Location?
2. Function?

Answer 13

IgE:

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

Question 14

Hypersensitivity:

5 types?

Answer 14

Hypersensitivity:

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

Question 15

Hypersensitivity:

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

Answer 15

Hypersensitivity:

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

Question 16

Hypersensitivity:

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

Answer 16

Hypersensitivity:

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

Question 17

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 ____.

Answer 17

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

Question 18

Chronic inflammatory disease examples?

Answer 18

Peptic ulcer disease, asthma, osteoarthritis, and gout

Question 19

Phases of the inflammatory response:

What are the 5 phases?

Answer 19

Phases of the inflammatory response:

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

Question 20

Phases of the inflammatory response:

Leukocyte infiltration:

4 stages?

Answer 20

Phases of the inflammatory response:

Leukocyte infiltration:

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

Question 21

Phases of the inflammatory response:

Leukocyte infiltration:

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

Answer 21

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

Question 22

Mediators that cause vasodilation?

Answer 22

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

Question 23

Mediators that increase vascular permeability?

Answer 23

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

Question 24

Chemotaxis and leukocyte activation mediators?

Answer 24

Chemotaxis and leukocyte activation:

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

Question 25

Tissue damage mediators?

Answer 25

Tissue damage mediators: a. Neutrophil/macrophage lysosomal products b. Oxygen radicals c. NO

Question 26

Mediators of fever?

Answer 26

Fever mediators: a. IL-1 b. IL-6 c. TNF d. PGE2

Question 27

Pain/hypersensitivity mediators?

Answer 27

Mediators of pain/hypersensitivity: a. PGE2/PGI2 b. Bradykinin c. Tryptase d. ATP

Question 28

2 strategies for drugs that target the immune system?

Answer 28

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

Question 29

Drug strategies for suppressing immunity/inflammation: Drug example: 1. Inhibition/activation of gene expression? 2. Blockade of intracellular signalling? 3. Costiumlation modulation?

Answer 29

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

Question 30

Drug strategies for suppressing immunity/inflammation: Drug example: 1. Receptor antagonism? 2. Chemical neutralization? 3. Blockade of synthesis?

Answer 30

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

Question 31

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?

Answer 31

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

Question 32

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?

Answer 32

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

Question 33

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?

Answer 33

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

Question 34

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

Answer 34

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

Question 35

Immunosuppressants: Drugs acting on immunocompetent cells?

Answer 35

Immunosuppressants: Drugs acting on immunocompetent cells: a. cyclosporine b. tacrolimus c. mycophenolate mofetil d. muromonab e. sirolimus

Question 36

Immunosuppressants: Drugs acting on cytokines or their receptors?

Answer 36

Immunosuppressants: Drugs acting on cytokines or their receptors: a. Daclizumab b. Infliximab c. Lenalidomide d. Etanercept e. Thalidomide

Question 37

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

Answer 37

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_

Question 38

Azathioprine: 1. Uses? 2. Major side effects?

Answer 38

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

Question 39

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

Answer 39

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_

Question 40

Glucocorticoids: Name several.

Answer 40

Glucocorticoids: hydrocortisone, cortisone, _prednisone_, prednisolone, methylprednisolone, dexamethasone, betamethasone, beclamethasone, fludricortisone, and aldosterone

Question 41

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?

Answer 41

Glucocorticoids: 1. Prevent and treat transplant rejection 2. High doses of _methylprednisone_ for acute rejection 3. Efficacious in GVHD and autoimmune disorders (Antiinflammatory properties)

Question 42

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?

Answer 42

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_

Question 43

Glucocorticoids: 4 mechanisms of action: 3. Cause __ cells to express smaller amounts of? This leads to decreased ___ synthesis and decreased amount of active ___ cells. 4. _Antiinflammatory_: decreased ____ production and decreased ____ expression.

Answer 43

Glucocorticoids: 4 mechanisms of action: 3. 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) 4. _Anti-inflammatory_: decreased _ecosanoid_ production and decreased _COX_ expression

Question 44

Glucocorticoids: 1. Site of action? 2. Metabolism? 3. Extensive long-term use is limited by \_\_\_\_.

Answer 44

Glucocorticoids: 1. Site of action: glucocorticoid response elements in DNA 2. CYP3A 3. Limited use bc of _toxicity_

Question 45

Antithymocyte Globulin (ATG) 1. What is this? 2. MOA: contains ___ to __ cell antigens and thus depletes?

Answer 45

Antithymocyte Globulin (ATG) 1. _Polyclonal antibodies_ 2. Contains _antibodies_ to _T_-cell antigens and thus depletes circulating T cells

Question 46

Antithymocyte Globulin (ATG) Used for what 4 things?

Answer 46

Antithymocyte Globulin (ATG) Used for: a. _induction of immunosuppression_ b. acute renal rejection c. aplastic anemia d. prevent GVHD

Question 47

Antithymocyte Globulin (ATG) 1. Can be used for withdrawl of ____ \_\_\_\_. 2. Often used in cases where ____ resistance occurs

Answer 47

Antithymocyte Globulin (ATG) 1. Withdrawl of _calcineurin inhibitors_ 2. Often used in cases where _steroid_ resistance occurs

Question 48

Antithymocyte Globulin (ATG) What is its most major side effect? And why? Other SE? Life threatening?

Answer 48

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)

Question 49

Cyclosporine: 1. What does it inhibit? 2. Use?

Answer 49

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

Question 50

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

Answer 50

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

Question 51

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

Answer 51

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

Question 52

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?

Answer 52

Cyclosporine: Toxicity: 1. Majority: _nephrotoxicity_ 2. 50% renal transplant patients: hypertension 3. Other: hirsutism, gum hyperplasia, tremor, hyperlipidemia, hepatotoxicity, and cancer

Question 53

Cyclosporine: Drug interactions: 1. What causes enzyme induction of hepatic metabolism? 2. What causes enzyme inhibition in hepatic metabolism? 3. Contraindication? Why?

Answer 53

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

Question 54

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

Answer 54

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

Question 55

Tacrolimus: MOA: Inhibits __ lymphocyte activation by forming complexes with intracellular protein \_\_\_\_. This complex then inhibits ___ and decreases ___ production by __ cells.

Answer 55

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

Question 56

Tacrolimus: Side effects?

Answer 56

Tacrolimus: Nephrotoxicity and neurotoxicity (like cyclosporine) Others: hyperglycemia, diabetes, cardiac hypertrophy, hypomagnesia, hyperkalemia

Question 57

Tacrolimus: Drug interactions: 1. Enzyme inducers? 2. Enzyme inhibitors? 3. Contraindications?

Answer 57

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

Question 58

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

Answer 58

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

Question 59

Sirolimus: 1. Use? 2. Metabolism? Absorption? T1/2?

Answer 59

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

Question 60

Sirolimus: Main side effects? How are the side effects dissimilar to calcineurin inhibitors?

Answer 60

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

Question 61

Mycophenolic Acid and Mycophenolate Mofetil: 1. Mycophenolic acid inhibits what? Why is this important? 2. Type of enzyme inhibition?

Answer 61

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

Question 62

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)

Answer 62

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

Question 63

Mycophenolic Acid and Mycophenolate Mofetil: 1. Uses? What can it be used with? Not used with? 2. Major side effects?

Answer 63

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

Question 64

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 \_\_\_\_)

Answer 64

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_)

Question 65

Muromonab-CD-3 (OKT3): 1. What is this? 2. Depletes available pool of?

Answer 65

Muromonab-CD-3 (OKT3): 1. _Mouse monoclonal antibody_ against human CD3 2. Depletes available pool of _T-cells_

Question 66

Muromonab-CD-3 (OKT3): MOA: _Prevents_ \_\__ cell activation and \_\_\_\_\_\_\__ by binding the receptor complex present on all _\_\_\_\_\_\__ _\_\_\__ cells causing apoptosis

Answer 66

Muromonab-CD-3 (OKT3): MOA: _Prevents T cell activation and proliferation_ by binding the receptor complex present on all _differentiated T_ cells causing apoptosis

Question 67

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)

Answer 67

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

Question 68

Daclizumab: 1. What is this? 2. Indication? 3. Why is this good?

Answer 68

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

Question 69

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

Answer 69

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

Question 70

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

Answer 70

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

Question 71

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

Answer 71

Etanercept: 1. _TNF alpha inhibitor_; binds TNF and functions as a _decoy receptor_ 2. Uses: RA and psoriasis 3. SE: infection, HepB, MS, seizures

Question 72

Lenalidomide: 1. Induces tumor cell \_\_\_\_\_. Also inhibits what? 2. Uses? 3. Side effects?

Answer 72

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

Question 73

Thalidomide: 1. Today's medical uses? 2. MOA? 3. SE?

Answer 73

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

Question 74

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?

Answer 74

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