Inflammation #5 RA Drugs Flashcards Preview

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Flashcards in Inflammation #5 RA Drugs Deck (45):
1

Which medication works by DHFR inhibition? How?

-Methotrexate
- DHFR inhibition causes reduction of tetrahydrofolate which reduces PURINE formation which leads to NO DNA synthesis.

2

What type of AIF effects does methotrexate have on RA?

It release/activates A2 receptors

3

A2 receptor stimulation cause the increase of _____ and the decrease of ______.

Increase of anti-inflammatory substances
- IL-10, IL-1Ra, sTNFR, Cholinergic AIF Pathway

Decrease inflammatory response
- Cytokines (TNF, IL-17, IL-1 etc..)
- Th-1, Th-17 cells
- MMPase activity
- COX-2 production + 5-LO production

4

What drug acts similarly to methotrexate w/ only once difference?
What's the difference?

Leflunomide (Arava)

- DOH (dihydrofolate) reductase inhibition
-no pyrimidines
-no DNA sythesis
-no T-cell activation + proliferation

5

In the absence of DNA synthesis, what cascade of events occurs?

- NO...
- T-cell activation (differentiation/ clonal expansion)
- B-cell formation
- RF
- Immune complexes
- Neutrophils
-macrophages/monocytes

6

If macrophages /monocytes aren't present in the cell then what CAN NOT occur?

Synthesis and Release of cytokines (IL-2, TNF, IL-1, IL-17)
- no neutrophils

7

What drug works by antigen processing inhibition? How?

Hydrochloroquine (Plaquenil)
- readily crosses the plasma membrane (macrophages) and increases pH from 4-6 (immune response) which INHIBITS auto-antigen interaction between MHCII molecules and auto-
antigens (AIF) response which to no antigen presentation

8

T/F? Plaquenil is acidic.

False
-basic

9

What 3 things do we need to know about Leflunomide (Arava)?

TOP: aspartate, asparagine, glutamate, and glumatine metabolism

MIDDLE: DHO dehydrodgenase

BOTTOM: pyrimidines

10

______ works by building up in lysosomes and inhibiting enzymes.

Hydroxychloroquine (Plaquenil)

11

What causes enzyme inhibition in the lysosome when using Hydroxychloroquine?

The increase in pH due to hydroxychloroquine being basic.

12

What 3 drugs are primarily used to treat Lupus?

-Cyclosporine
- D-Penicillamine
-Cyclophosphamide

13

What 3 drugs are have UNKNOWN MOAs?

-Minocycline
-Sulfasalazine
-D-Penicillamine

14

What is the MOA of Gold Salts?

a. unknown
b. decrease in T-cell activation + proliferation
c. General immunosuppressant, IL-2 inhibition
d.cross linking DNA chains to reduce lymphocyte (B-cells) proliferation

b. decrease in T-cell activation + proliferation

15

What is the MOA of Cyclosporine?

a. unknown
b. decrease in T-cell activation + proliferation
c. General immunosuppressant, IL-2 inhibition
d.cross linking DNA chains to reduce lymphocyte (B-cells) proliferation

c. General immunosuppressant, IL-2 inhibition

16

What is the MOA of D-Penicilliamine?

a. unknown
b. decrease in T-cell activation + proliferation
c. General immunosuppressant, IL-2 inhibition
d.cross linking DNA chains to reduce lymphocyte (B-cells) proliferation

a. unknown

17

What is the MOA of Cyclophosphamide?

a. unknown
b. decrease in T-cell activation + proliferation
c. General immunosuppressant, IL-2 inhibition
d. cross linking DNA chains to reduce lymphocyte (B-cells) proliferation

d.cross linking DNA chains to reduce lymphocyte (B-cells) proliferation

18

What drug works by producing LOW FUNCTIONING DNA therefore decreasing T-cell and B-cell activation? How?

Azathioprine (Imuran)
- purine analog

19

What drug works by suppressing activation of lymphocytes? How?

Tofacitnib (Xeljanz)
- by inhibiting JAK/STAT inhibitor

20

Xeljanz binds to _____ in order to produce its affects?

-phosphorylation site of the cytokine receptor and prevents STAT from entering the nucleus (transcription + translation) and releasing cytokines. (IL-2, IFN (t-cell activation), etc..)

21

Name the 4 monoclonal anti-body TNF inhibitors.
What do they do?

Certolizumab (Cimzia): Fab fragment
Infliximab (Remicade): chimeric
Golimumab (Simponi): human
Adalimumab (Humira): human

-By binding to TNF and preventing access of TNF to its receptor yielding "No Response"

22

JAK/STAT pathway:
________ binds to the cytokine receptor causing dimerization of the ________. This leads to the activation and auto-phosphorylation ___________ which allows for the ________ of STAT which is then translocated to the nucleus to cause transcription/translation. leading to the up regulation of inflammatory mediators.

-cytokine
-receptor
- JAK
- phosphorylation/
dimerization

23

Name the 1 TNF antagonist that is considered a fusion protein? Why is it considered a fusion protein?

Etanercept (Enbrel)
-

24

Name the 2 medications that bind to the TNF receptor (competitive antagonist)?

Anakinra (IL-1)
Tocilizumab (Actemra) (IL-6)

25

Which of the following monoclonal antibody types is MOST likely to be immunogenic by itself? LESS likely?

a. mouse
b. chimeric
c. humanized
d. human

a. mouse (MORE side effects)

c. humanized (LESS) side effects

26

What TNF inhibitor/antagonists has a PEGylated Fab region?

Certolizumab (Cimzia)

27

What is the overall effect of PEGylation?

LONGER 1/2 LIFE

28

How does Certolizumab (Cimzia) exert its longer 1/2 life effects (3)?

via PEGylation
- reduces proteolysis + kidney excretion
- increases affinity of drug

29

T/F?
What drug decreases immunogenicity?

Certolizumab (Cimzia)

30

If TNF is suppressed what is still active and enables the body to still undergo the positive effects of inflammation?

IL-17

31

What drug binds to IL-1 receptors to prevent activation of NFkB pathway?

Anakinra (Kineret)

32

Which of the following drugs is an TNF antagonist?

a. Anakinra (Kineret)
b. Etanercept (Enbrel)
c. Tocilizumab (Acetmra)
d. Rituximab (Rituxan)

b. Etanercept (Enbrel)

33

Which of the following drugs is an IL-1 receptor antagonist?

a. Anakinra (Kineret)
b. Etanercept (Enbrel)
c. Tocilizumab (Acetmra)
d. Rituximab (Rituxan)

a. Anakinra (Kineret)

34

Which of the following drugs is an cause B-cell depletion?

a. Anakinra (Kineret)
b. Etanercept (Enbrel)
c. Tocilizumab (Acetmra)
d. Rituximab (Rituxan)

d. Rituximab (Rituxan)

35

Which of the following drugs is an IL-6 antagonist?

a. Anakinra (Kineret)
b. Etanercept (Enbrel)
c. Tocilizumab (Acetmra)
d. Rituximab (Rituxan)

Tocilizumab (Actemra)

36

Which of the following combinations would lead to serious opportunistic infections? Why?

a. Etanercept + Anakinra
b. Etanercept + Infliximab (Remicade)
c. Etanercept + Golimumab (Simponi)
d. Etanercept + Certolizumab (Cimzia)

a. Etanercept + Anakinra

- blocking TNF and IL-1

37

What drug is a soluble fusion protein of CTLA4 and the Fc region of monoclonal antibody?

Abatacept (Orencia)

38

Which of the following agents block the formation of the co-stimulation signals required for T-cell activation via CTLA4?

Abatacept (Orencia)

39

MOA of Abatacept (Orencia) (3)

-Binds to B7 (macrophage- APC) via CTLA4 --> inhibits T-cell activation, proliferation, differentiation

- NO T-cell activation --> NO B-cell activation

- Decreases cytokines (IL-2, 6, RF, CRP, MMP, and TNF)

40

_____ has a higher affinity for B7 than CD28.

CTLA4

41

What protein is known to be an early marker for normal + malignant B-cells?

CD 20

42

What non-TNF biologic agent is administered w/ methotrexate?

Rituximab (Rituxan)

43

What can destroy a B-cell? How?

- binding to the CD20 protein on a B-cell

- causing antibody-dependent cellular cytotoxicity
(ADCC) and complement-dependent cytotoxicity (CDC)

44

Which of the following agents is associated with lysis of B-cells and depletion?

a. Anakinra (Kineret)
b. Etanercept (Enbrel)
c. Rituximab (Rituxan®)
d. Rituximab (Rituxan)

c. Rituximab (Rituxan®)

45

What drug binds to the IL-6 receptor?

Tocilizumab (Actemra®)