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Block 7; Week 5-Michelle > Duan-DMARDS etc > Flashcards

Duan-DMARDS etc Flashcards

1
Q

What are the important corticosteroids to keep in mind?

A

prednisone
prednisolone
dexamethasone

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2
Q

What are some important DMARDs that are anti-TNFalpha?

A

adalimumab
infliximab
etanercept
anakinra

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3
Q

What are some important DMARDs that are antimetabolites?

A

azathioprine
methotrexate
cyclophosphamide
cyclosporine

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4
Q

What are the symptoms of RA? How would you describe this disease?

A

chronic progressive systemic autoimmune disease
Symmetric synovitis
Joint inflammation, pain, swelling, stiffness, progressive erosions of bones, joint misalignment, reduced or lost function
rheumatoid nodules on the extensor surfaces of the elbows, forearms, and hands.
Multisystem extra-articular manifestations
Pulmonary and vascular involvement
Keratoconjunctivitis
Sensory peripheral neuropathy

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5
Q

What are the goals of RA therapy?

A

Control inflammation
Alleviate pain
Slow progression/rate of joint damage
Reduce disease activity and induce remission
Maintain function for essential daily activities
Maximize quality of life

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6
Q

What are the ways to admin RA meds? Other treatments?

A

systemic oral meds
intra-articular injections
joint exercises & rest
joint surgery

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7
Q

What are the 2 functional groups that RA medicines fall into?

A
  1. drugs that treat pain & inflammation but don’t limit joint damage
  2. drugs that help control disease & limit joint damage
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8
Q

Where do NSAIDS & Corticosteroids (glucocorticoids) & DMARDS fall into functional categories?

A

NSAIDS & Corticosteroids–drugs that treat pain & inflammation
DMARDS–limit joint damage

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9
Q

What is combination therapy?

A 
widely used
several oral DMARDS
OR
oral + biological DMARDS
OR
DMARDS + Corticosteroids (systemic or injection)
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10
Q

Phospholipase A2 turns Membrane phospholipids into eicosanoids. Which 2 enzymes are involved next?

A

LOX: turns eicosanoids into leukotrienes.
COX: turns them into prostaglandins.

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11
Q

What are some drugs that target Phospholipase A2?

A

Corticosteroids: prednisone & dexamethasone

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12
Q

What are some drugs that target COX?

A

NSAIDS

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13
Q

Which drugs target LOX?

A

5-lox inhibitors
sulfasalazine
leukotriene receptor antagonist

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14
Q

What does the presence of leukotrienes do? Prostaglandins cause inflammation.

A

phagocyte mobilization
changes in vascular permeability
inflammation

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15
Q

Which enzyme, COX-1 or COX-2 causes inflammation, pain, fever?

A

COX-2

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16
Q

What are the advantages of using NSAIDs to manage RA?

A 
effective control of inflammation & pain
effective reduction in swelling
improves mobility, flexibility, ROM
QOL up
low cost
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17
Q

What are the disadvantages of using NSAIDS to manage RA?

A 
doesn't help disease progression
GI toxicity possible
renal problems
hepatic dysfunction
CNS toxicity with high dose
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18
Q

Where are corticosteroids made in the body?

A

adrenal cortex

including glucocorticoids & mineral corticoids

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19
Q

What is the function of glucocorticoids? WHat is an example?

A

cortisol
carb, fat, protein metabolism
prevent phospholipid release-anti-inflammatory
decrease eosinophil action

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20
Q

What is the function of mineral corticoids? What is an example?

A

Aldosterone
electrolyte & water levels
promotes sodium retention in kidney

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21
Q

Describe the hypothalamic-pituitary adrenal axis feedback.

A

CRH (vasopressin) from hypothalamus stimulates Pituitary gland to release ACTH.
ACTH causes the release of Glucocorticoids from adrenal glands.
Neg feedback to pituitary & hypothalamus.
Pos feedback to hippocampus, which is inhibitor to hypothalamus.
Additionally, stress is stimulatory to hypothalamus.

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22
Q

What is the MOA of corticosteroids?

A

diffuse into cells via simple diffusion & binds transcription factors. Enter nucleus & regulate synthesis of IFNgamma, GM-CSF & interleukins & TNFalpha
also inhibit COX-2 & phospholipase A2.

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23
Q

How do corticosteroids use lipocortin?

A

lipocortin inhibits phospholipase A2.

Corticosteroids increase lipocortin.

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24
Q

What are some clinical uses of glucocorticoids?

A 
immunosuppression
anti-inflammatory
autoimmune diseases (RA)
Asthma
Anti-cancer
Replacement THerapy (addison's disease)
Allergic disorders
collagen disease
nephrotic disease
resp distress syndrome
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25
Name some corticosteroids used in RA therapy? Which have short duration? Long duration?
``` Cortisol: 1.5-3 hrs Cortisone: 0.5 hrs Prednisone: 3-4 hrs Triamcinolone: 36-54 hrs Dexamethasone: 35-54 hrs Fludrocortisone: 24 hrs ```
26
How do synthetic corticosteroids compare to endogenous ones?
Synthetic have stronger potency, lower dose, longer duration
27
How are corticosteroids well absorbed? How do they travel in blood? Where are they metabolized? Excreted?
well absorbed orally bound to plasma proteins metabolized in liver (Cyt P450) excreted in kidney
28
What are some other important pharmacokinetic features of corticosteroids?
Plasma half-life shorter than biological halflife Substantial lag time before onset of action Persistence of effect after disappearance from plasma
29
What are the adverse effects of using chronic use of glucocorticoids?
``` Fat redistribution: Cushing's syndrome, Moon face, buffalo hump Diabetes HPA suppression Impaired Wound Healing MSK: osteoporosis Cardio: fluid retention, edema, HTN Gastric Ulcers Infection Growth inhibition ```
30
What are the advantages of corticoid therapy?
anti-inflammatory & immunosuppression | helps joint flares if you use intra-articular injections
31
What are the disadvantages of corticoid therapy?
doesn't affect disease progression skin thinning, ecchymoses, Cushing appearance cause of steroid-induced osteopenia
32
What are oral DMARDS?
small molecular chemical drugs
33
What are biologic DMARDS?
genetically engineered antibodies & proteins Ex: TNFalpha blockers can also target IL-1, IL-6, CD20, CD28
34
How long does it take for DMARDS to have an observable clinical effect?
takes more than 3 months
35
What is the MOA of azathioprine?
purine synthesis inhibitor
36
What is the MOA of cyclosporin A?
calcineurin inhibitor
37
What is the MOA of leflunomide?
pyrimidine synthesis inhibitor
38
What is the MOA of methotrexate?
purine metabolism inhibitor
39
What is the MOA of abatacept?
T cell costimulatory signal inhibitor
40
What is the MOA of adalimumab?
TNF alpha inhibitor
41
What is the MOA of chloroquine & hydroxychloroquine? Note: these are antimalarials
suppression of IL-1 & TNFalpha | induce apoptosis of inflammatory cells & decrease chemotaxis
42
What is the MOA of D-penicillamine?
reducing numbers of T lymphocytes
43
What is the MOA of etanercept & golimumab? And infliximab
TNFalpha inhibitor
44
What is the MOA of minocycline?
5-LO inhibitor
45
What is the MOA of rituximab?
chimeric monoclonal antibody against CD20 on B-cell surface
46
What is the MOA of sulfasalazine?
Suppression of IL-1 & TNF-alpha, induce apoptosis of inflammatory cells and increase chemotactic factors
47
What is the MOA of tocilizumab?
anti-IL6
48
What is the recommended dose for methotrexate in treatment of rheumatoid arthritis?
7.5-20 mg/wk
49
What are the advantages to DMARDS?
``` slow disease progression improve functional disability decrease pain interfere with inflammation retard joint erosions ```
50
What is the time to benefit for methotrexate?
1-3 mo
51
What is the potential toxicity for methotrexate?
moderate | on par with gold (parenteral)
52
What are the toxicities to monitor for DMARDs?
hepatotoxicity pulmonary myelosuppression
53
What is the general & specific MOA for methotrexate?
general: purine metabolism inhibitor specific: blocks dihydrofolate reductase & thymidylate synthase
54
What are the pros of using methotrexate?
we know what it does ok to continue therapy with it proven efficacy in RA
55
What are the cons of using methotrexate?
lab monitoring every 1-2 mo | possible liver, lung toxicity, myelosuppresion
56
What is the MOA of sulfasalazine?
COX & LOX inhibitor as well as IL-1 & TNFalpha inhibitor
57
What are the pros to sulfasalazine?
effective | mild level of toxicity
58
What are the cons to using sulfasalazine?
some pts sulfa intolerant bad for patients with G6pd deficiency monitor every 3 mo look for myelosuppression, GI, decreased digoxin absorption
59
What is the MOA of azathioprine?
immunosuppressive purine synthesis inhibitor prevents leukocyte proliferation
60
What are the pros to azathioprine?
effective in refractory RA | metabolized to 6-mercaptopurine
61
What are the cons to azathioprine?
risk for severe leukopenia, thrombocytopenia risk for liver toxicity, cancer, opportunistic infections, macrocytic anemia, bone marrow depression, GI have to monitor every 2 weeks & then every 1-3 mo.
62
What shouldn't you take azathioprine with for risk of myelosuppresion?
ACE-1 inhibitor or allopurinol for gout.
63
What is the MOA of gold auranofin?
blocks phagocytosis
64
What are the pros of gold auranofin?
good for refractory RA can be used orally accumulates in synovium
65
What are the cons of gold auranofin?
6 mo before you know if effective close monitoring can't take if you have liver or kidney problems can't combine with other immunosuppressants shouldn't use with X-rays
66
What are the some of the toxicities associated with gold auranofin?
``` skin lesions stomatitis oral ulcers glomerulonephritis nephrosis thrombocytopenia agranulocytosis ```
67
What is the MOA of leflunomide aka ARAVA?
inhibits pyrimidine biosynthesis by inhibiting dihydroorotate dehydrogenase (mitochondrial enzyme) affects T cells
68
What are the pros of lefluonomide aka arava?
works in 1 mo can use long term prevents expansion of activated lymphocytes selectively targets autoimmune lymphocytes
69
What are the cons of lefluonomide?
less clinical experience with it liver & GI toxicity expensive long half life requires loading
70
Once again, what are biological DMARDS?
genetically engineered antibodies & proteins | block cytokines & signaling molecules
71
What are the biological TNF alpha blockers?
Adalimumab (Humira) Etanercept (Enbrel) Infliximab (Remicade)
72
What is the biological DMARD that blocks IL-1?
anakinra (kineret)
73
What is the biological DMARd that blocks B cells CD20?
Rituximab (Rituxan)
74
What is the structure of etanercept (enbrel)? Which drug is it sometimes used with? How is it administered?
dimeric fusion protein extracellular ligand that binds TNFreceptor that is linked to the Fc part of IgG1 used sometimes with methotrexate administered by injection
75
What seems to be the main problem with Etanercept?
immunosuppressive can get bad infections don't use in diabetics etc.
76
WHat is the structure of infliximab aka remicade?
chimeric IgG1 antibody that binds to TNFalpha with high affinity inhibits binding of TNFa to receptors by bind to it first! can be used with methotrexate
77
T/F Methotrexate could potentiate the antirheumatoid activity of infliximab while reducing its immunogenicity
True.
78
What is the structure of adalimumab aka Humira?
recombinant IgG1 monoclonal antibody specific for TNFalpha only consists of human peptide sequences binds TNFalpha & blocks its interaction w/ p55 & p75 on cell surfaces
79
When would you prescribe a biologic DMARD over an oral DMARD?
for patients with longstanding active RA that need to change their therapy give a greater symptoms response & remission rate than oral DMARDS can't compare effectiveness yet
80
IS it okay to combine 2 biologic DMARDS?
NO. doesn't increase effectiveness | increases risks for bad side effects
81
What are some good DMARD combos?
methotrexate + sulfasalazine + hydroxychloroquine methotrexate + cyclosporine methotrexate + leflunomide methotrexate + biologic DMARD **only for people with longstanding active RA, not early RA
82
T/F DMARDS should be initiated early in active RA.
True.
83
T/F DMARD combo treatment should be X + sulfasalazine.
False. X + methotrexate
84
T/F Biologic DMARDs are indicated when oral DMARDs are not successful.
True.
85
T/F Biologic DMARDs + Methotrexate are superior to oral DMARDs + methotrexate.
False. superior to oral DMARDS alone...that's all we know for now.
86
What is an effective firstline treatment for RA?
Methotrexate (oral DMARD)
87
For people with longstanding active RA...what do you sometimes want to do with oral DMARDs?
use 2-3 oral DMARDs at once!

Block 7; Week 5-Michelle (11 decks)

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