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Rheum > 01b: Pharmacology > Flashcards

01b: Pharmacology Flashcards

1
Q

(Biologics/non-biologics) are referred to as DMARDs and typically have MW (over/under) (X).

A

Non-biologics;
Under
X = 1000 Da

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2
Q

Biologics are typically (X) molecules that are administered via which routes?

A

X = IgG

IV or SC

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3
Q

Hydroxychloroquinone is in (X) class of immunosuppressants and works via which mechanisms on (Y) cells?

A 
X = antimalarial (non-biologic)
Y = synovial fibroblasts and B cells
  1. Sensitization to Fas-induced apoptosis
  2. Inhibition of TLR-dependent cell activation
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4
Q

Hydroxycholorquinone is used as immunosuppressant in which diseases?

A

Lupus, mild RA

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5
Q

Side effects of Hydroxycholorquinone.

A

Accumulation in/damage to retina (requires ophthalmologic monitoring)

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6
Q

T/F: One advantage of Hydroxycholorquinone is its very low potential for toxicity at lower doses.

A

True

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7
Q

Sulfasalazine is in (X) class of immunosuppressants and reduces inflammation by which mechanism?

A

X = 5-aminosalicylates (non-biologics)

Parent drug increases level of adenosine

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8
Q

Sulfasalazine DMARD effect is by which actions on which cells?

A
  1. Suppress T cell function (IkkB inhibition blocks NFkB signaling)
  2. Inhibit B cell proliferation
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9
Q

Sulfasalazine is effective in (X) diseases with (greater/less/same) efficacy as hydroxychloroquine.

A

X = RA and spondyloarthropathies

Greater

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10
Q

(X) (biologic/non-biologic) immunosuppressant drug should be avoided in patients with G6PD deficiency due to (Y) adverse effect.

A

X = sulfasalazine
Non-biologic

Y = hemolytic anemia

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11
Q

Methotrexate is (biologic/non-biologic) that works by which mechanism at high doses?

A

Non-biologic

Inhibits TMP (thymidine monophosphate) synthesis, thus DNA replication/cell division; anti-neoplastic effect

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12
Q

Methotrexate is in (X) class of DMARDs that works by which mechanism at low doses?

A

Purine synthesis inhibitors;

Inhibits DHF Reductase (de novo purine synthesis); anti-rheumatic effect; also increase adenosine (anti-inflammatory)

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13
Q

List some side effects of methotrexate.

A
  1. Nausea and mucositis

2. Hepatotoxicity

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14
Q

T/F: Switching from parenteral to oral administration of methotrexate may decrease nausea/hepatotoxicity.

A

False - vice versa

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15
Q

Folate supplementation has been shown to (increase/decrease) effects of (X) immunosuppressant drug.

A

Decrease;

X = methotrexate

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16
Q

(X) immunosuppressant is teratogenic and used to induce abortion. Thus, which patients should avoid using it?

A

X = methotrexate

Pregnant women or men considering fatherhood

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17
Q

Aside from high dose, list some circumstances that might increase the side effect risks of methotrexate in a patient.

A

Reduced renal clearance:

  1. Renal disease
  2. Use of OATP inhibitors
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18
Q

Methotrexate is drug of choice for which rheumatic diseases? Star the one it’s especially effective for.

A
  1. RA*
  2. Lupus
  3. Vasculitis
  4. Psoriatic arthritis and others
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19
Q

(X) is in (Y) class of immunosuppressants that is active once the prodrug is metabolized into 6-mercaptopurine (6-MP).

A 
X = Azathioprine
Y = purine synthesis inhibitors (non-biologics)
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20
Q

6-mercaptopurine has (X) effect on B cells and (Y) effect on T cells.

A 
X = inhibits DNA replication (blocks IMP synthesis)
Y = inhibits DNA replication AND initiates T cell apoptosis
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21
Q

(X) prodrug is metabolized into 6-mercaptopurine (6-MP) and then to nucleotides by (Y).

A 
X = Azathioprine
Y = HGPRT (hyopxanthine quanine phosphoribosyl transferase)
22
Q

List the three main side effects of azathioprine.

A
  1. Bone marrow suppression
  2. Infection
  3. Malignancy
23
Q

Risk of azathioprine side effects is increased by:

A

Deficiency in TPMT (thiopurine methyltransferase) enzyme, which inactivates 6-MP

24
Q

Leflunomide is in (X) class of immunosuppressants and acts by which mechanism?

A

X = pyrimidine synthesis inhibitors (non-biologics)

Converted to active metabolite that inhibits dihydroorotate dehydrogenase (inhibits T/B cell de novo pyrimidine synthesis)

25
Q

Therapeutic (anti-rheumatic) uses for Azathioprine:

A

SLE, myositis, vasculitis

26
Q

Leflunomide risk of (X) side effect is increased when it’s used in combo with methotrexate.

A

X = hepatotoxicity

27
Q

(X) DMARD used to treat RA has long half-life and undergoes enterohepatic circulation. An overdose of this drug can be effectively treated with (Y).

A 
X = Leflunomide
Y = cholestyramine (bile acid binding resin to increase fecal clearance)
28
Q

Cyclophosphamide is in (X) class of immunosuppressants. It’s (activated/inactivated) via metabolism by (Y).

A

X = DNA Alkylating agent
Activated (into phosphoramide mustard)
Y = Hepatic CYP450s

29
Q

(X) DMARD is a prodrug that is metabolized into phosphoramide “mustard”. What’s the mechanism of action of this active metabolite?

A

X = cyclophosphamide

Cross-links DNA (alkylating agent) that blocks cell replication

30
Q

Cyclophosphamide used to treat which rheumatic diseases?

A
  1. SLE and scleroderma (esp pulm fibrosis)

2. Vasculitis

31
Q

T/F: Cyclophosphamide typically used in combo with Methotrexate for RA.

A

False - used in combo with glucocorticoids; NOT used for RA

32
Q

Cyclophosphamide side effects:

A
  1. Bone marrow suppression
  2. Infertility
  3. Alopecia (hairloss)
33
Q

Glucocorticoids mechanisms of immunosuppression include:

A
  1. Increase IkB transcription, which binds/blocks NFkB
  2. Inhibit cytokine secretion (phages and T cells)
  3. Inhibit B and T cell replication
34
Q

T/F: Low-dose corticosteroids for 6 months are recommended in RA.

A

True - ideally less tho

35
Q

JAK3 is a(n) (X) molecule that’s expressed in (Y) cells. It contributes to:

A 
X = enzyme
Y = T and B cells

Signaling of cytokines (like IL-2)

36
Q

List the three classes of biologics used for immunosuppression (anti-rheumatic).

A
  1. Cytokine (IL-1/6, TNFa) antagonists
  2. T-cell costimulation inhibitor
  3. Anti-CD20 B cell depleter
37
Q

Adalimumab is in (X) class of immunosuppressants and has which structure/mechanism?

A

Fully humanized IgG; binds TNFa with high affinity and blocks interaction with receptor

38
Q

TNFa antagonists are approved for which rheumatic diseases?

A
  1. RA
  2. Psoriatic arthritis/psoriasis
  3. Ankylosing spondylitis
39
Q

T/F: Patients on TNFa antagonists must go get injections at inpatient/outpatient clinic.

A

False - preloaded devices can be bought for self administration (SC injection)

40
Q

List some important side effects of Adalimumab.

A
  1. TB REACTIVATION (test for TB prior to use)
  2. Injection site reaction
  3. CHF aggravation
  4. AutoAb development (lupus-like syndrome)
41
Q

Abatacept is in (X) class of immunosuppressants and has which structure?

A

X = T cell co-stimulation inhibitors

Fusion protein (IgG Fc portion with extracellular domain of CTLA4)

42
Q

Abatacept is binds (X) and (stimulates/inhibits) (Y).

A

X = APC (B7)
Inhibits
Y = Interaction with CD28 on T cell

43
Q

Abatacept side effects:

A
  1. Infusion-related reactions
  2. Infections
  3. Antagonism of immunizations
44
Q

Abatacept should not be used in combo with (X) because there’s an increased risk of (Y) adverse effect without an increase in therapeutic response.

A 
X = anti-TNFa drugs
Y = infection
45
Q

Live vaccines must not be given prior to/during use of (X) immunosuppressant drug.

A

X = abatacept

46
Q

Patient with RA is not responding to DMARDs. What (in order) are the next two drugs you would try.

A
  1. Adalimumab (TNFa antagonists)

2. Abatacept (T cell co-stim inhibitor) OR Rituximab (B cell depleter)

47
Q

Rituximab is in (X) class of immunosuppressants and has which structure?

A

X = Anti-CD20 B cell depleter

IgG binding with high affinity to CD20

48
Q

What is the effect of Rituximab binding to (X)?

A

X = CD20 on B cells

Complement or Ab-dependent cytotoxicity or apoptosis

49
Q

In early RA with low disease activity (X) (mono/combo)-therapy is preferred.

A

X = methotrexate

Monotherapy

50
Q

If RA disease activity remains moderate or high despite DMARD monotherapy, what options would you consider?

A
  1. DMARD combo

2. Biologic (anti-TNFa or other) with/without MTX

51
Q

T/F: In established RA with low disease activity MTX monotherapy is preferred over a anti-TNFa.

A

True

Rheum (6 decks)

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