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pharmacology 4810 > Arthritis & Gout MT2 > Flashcards

Arthritis & Gout MT2 Flashcards

1
Q

what is rheumatoid arthritis

A
  • autoimmune disease that causes chronic inflammation of the joints
  • affects joints first, then surrounding tissues may become affected
  • usually occurs between 40 and 60 years of age
  • 2 to 3 times more common in women
  • genetic basis
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2
Q

what type of disease is RA directly linked to?

A

cardiovascular disesae
- increase in MI, stroke, heart failure and hypertension than non-RA patients

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3
Q

what are some symptoms of RA

A
  • joint inflammation (swelling, redness, pain and stiffness)
    chronic inflammation can lead to damage and deformity of joints
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4
Q

what are some tests that may be done to diagnosis someone with rheumatoid arthritis

A
  • rheumatoid factor test
  • anti-CCP antibody test
  • complete blood count
  • CRP (C-reactive protein)
  • ESR (eryhtocyte sedimentation rate)
  • ultrasound/MRI/X-ray
  • synovial fluid analysis
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5
Q

what are some causes of RA

A
  • infectious agents that deposit into the joints and cause inflammation
  • genetic link/genetic inheritance
  • environmental factors (smoking)
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6
Q

what is the difference between the 1980 pyramid approach of treatment of RA and how RA is treated now

A

1980 pyramid approach was that topical NSAIDs and aspirin were on the bottom of the pyramid. 2nd line therapy was initiated after a patient had proven radiographic damage. RA was considered a nuisance disease and the treatment of the disease was worse than its natural course, therefore symptomatic treatment only.

currently, pharmacological intervention is necessary early in order to prevent structural damage. multi drug therapy is not only well tolerated but is necessary. the goal is to put disease into remission

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7
Q

what are some non-pharmacological treatment options for RA

A
  • patient education on nature of RA, coping mechanisms
  • physical and occupational therapy for joint-strengthening and joint protection
  • prevention of osteoporosis is RA and antiresorptive therapy for those who receive chronic corticosteroids
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8
Q

what are the “first line” drugs used to reduce inflammation in RA

A

NSAIDS and corticosteroids

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9
Q

what are the “second line” drugs used to promote remission of the disease and prevent progressive joint damage in RA

A

DMARDs and biologics or biologic response modifiers

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10
Q

corticosteroids are any of the steroidal hormones made by the _______ of the adrenal gland (e.g. cortisol)

A

cortex (outer layer)

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11
Q

true or false: steroids inhibit the synthesis of almost all known cytokines

A

true

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12
Q

what is the MOA of corticosteroids

A

they stimulate the synthesis of IF-kappa beta alpha, which is a protein that traps and therefore inactivates nuclear factor kappa B (NF-kB)

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13
Q

this is an activator of cytokine genes and mediator of the pro-inflammatory action of tumour necrosis factor and IL-1

A

nuclear factor kappa beta (NF-kB)

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14
Q

what are some possible side effects of corticosteroids

A
  • increased appetite and weight gain
  • deposits of fat in chest, face, upper back and stomach
  • swelling and edema due to water and salt retention
  • high blood pressure, diabetes
  • slower healing of wounds
  • black and blue marks
  • osteoporosis
  • increased susceptibility to infections
  • cataracts
  • muscle weakness
  • thinning of the skin
  • stomach ulcers
  • increased sweating
  • mood swings
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15
Q

what is the route of administration for corticosteroids

A
  • oral
  • topical (for eczema, allergic conjunctivitis, or rhinitis)
  • parenteral/injection
  • aerosol (for asthma)
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16
Q

do corticosteroids bind to proteins?

A

yes, bind to corticosteroid binding globulin (CBG) and albumin in the blood and then enter cells by diffusion

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17
Q

what is the half life of hydrocortisone

A

90 min. main effect lasts for 2-8 hrs

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18
Q

cortisone and prednisone are inactive until converted in vivo to ______________

A

hydrocortisone

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19
Q

what organ metabolizes corticosteroids

A

liver

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20
Q

what are some examples of medications that should be taken with NSAIDs to offset side effects

A

-antacids (Sucralfate)
- PPIs (lansoprazole, etc)
- PG analogues (misoprostol)

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21
Q

examples include methotrexate, chloroquine, hydroxychloroquine, sulfasalazine, leflunomide, biologics, gold salts, penicillamine, cyclosporin and cyclophosphamide

A

DMARDs - disease modifying anti-rheumatic drugs

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22
Q

this specific DMARD is classified as an anti-metabolite, but in RA the MOA seems more anti-inflammatory than anti-metabolite. it is an inhibitor of folate (vit. b6) metabolism

A

methotrexate (Rheumatrex, Trexall)

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23
Q

what is the MOA of methotrexate for RA

A
  • it inhibits leukotriene synthesis and dihydrofolate reductase
  • decreases TNF concentrations

net effect: a decrease in T and B cell proliferation and a decrease in rapidly dividing synoviocytes. there is promotion of apoptosis of activated peripheral T cells

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24
Q

how much methotrexate is absorbed orally

A

70% but variable depending on dose

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25
Q

in terms of distribution, how much methotrexate is bound to proteins

A

50% bound to plasma proteins

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26
Q

how and how fast is methotrexate excreted

A

primarily by urine within 48 hrs (clearance may be diminished in elderly and those with decreased renal fxn)

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27
Q

what are some side effects of methotrexate

A

contraindicated in pregnancy
- generally well tolerated, but may see some of the following SE’s with high doses
- mouth sores
- headaches
- dizziness
- hair loss
- stomtitis
- drowsiness
- itching, rash
- low WBCs
- folate deficiency
- accelerated rheumatoid nodulosis
- can also have severe liver and bone marrow toxicity, therefore patients need to be monitored

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28
Q

this is an isoxazole derivative

A

Leflunomide (Avara)

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29
Q

what the MOA of leflunomide

A

it completely inhibits dihydroorotate dehydrogenase which is required for de novo synthesis of pyrimidines. this blocks the proliferative lymphocyte response in inflammation

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30
Q

true or false: lefluonomide is a prodrug that is converted to active metabolite A77 1726

A

true

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31
Q

this is highly protein bound and has a half life of 15-18 days. it undergoes extensive enterohepatic recirculation. persisting drug levels seen 1-2 years after discontinuation. not recommended in patients with advanced renal disease

A

leflunomides active metabolite (A77 1726)

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32
Q

what are some adverse effects and side effects of leflunomide

A

adverse effects: hepatotoxicity. contraindicated in preganancy - d/c 2 years before attempts at pregnancy

side effects: diarrhea, hair loss, reduction in WBC and RBC, hypertension, peripheral neuropathy, itching, rash

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33
Q

this is generally used in the treatment of inflammatory bowel diseases such as UC and chrons, and used as an antimicrobial agent. it is converted by bacteria in the colon into 5-aminosalicylic acid (5-ASA) and sulfapyridine.

A

sulfasalazine (Azulfadine)

34
Q

what is the MOA of sulfasalazine

A
  • does not appear to inhibit COX even if 5-ASA is the therapeutic agent
    appears to inhibit TNF-alpha, IL-1 and NF-kB. also scavenges free radical and oxygen species
35
Q

what are some side effects of sulfasalazine

A

GI (N/V), dizziness, change in color of skin or urine, can cause reduction of WBCs and RBCs

36
Q

what is the MOA of chloroquine/hydroxychloroquine (Plaquenil)

A

suggested MOAs
- inhibits sulfhydryl-disulfide interchange (which is important for proliferation of immune cells)
- inhibits enzyme reactions (decreased phospholipase action)
- binds to DNA and interferes with replication in immune cells
- decreases chemotaxis, phagocytosis, fibroblast growth, and WBC proliferation

37
Q

this has a very favourable safety profile
- rapidly absorbed
- plasma levels plateau in 8-14 days
- long plasma half-life (3-10 days depending on dosing regimen)
- slow urinary excretion
- tissue levels are higher than plasma levels
- concentrates in pigmented ocular tissue

A

cloroquine/hydroxychlorquine (Plaquenil)

38
Q

what are some side effects of chloroquine/hydroxychloroquine (Plaquenil)

A

relatively safe
- GI
- skin and hair lesions
- muscle weakenss
- ocular defects (including retinopathy)

39
Q

true or false: combination of methotrexate and other compounds (such as leflunomide, sulfasalazine and hydroxychloroquine) is common

A

true

40
Q

this is a class of biologic response modifiers Etanercept (Enbrel), Infliximab (Remicade), Adalimumab (Humira), Certolizumab pegol (Cimizia), Golimumab (Simponi)

A

TNF inhibitors

41
Q

this is a class of biologic response modifiers
Abatacept (Orencia)

A

CTLA4 fusion to IgG1 (CD4 antagonist)

42
Q

this is a class of biologic response modifiers
Rituximab (Rituxan)

A

chimeric, anti CD20 monoclonal antibodies

43
Q

this is a class of biologic response modifiers
anakinra (Kineret)

A

IL-1 receptor inhibitors

44
Q

this is a class of biologic response modifiers
Tocilizumab and Sarilumab

A

IL-6 receptor inhibitors

45
Q

_________ are a class of drugs that work by blocking the action of janus kinase enzymes which are involved in the inflammation that causes the symptoms of RA

A

JAK inhibitors

46
Q

this is a JAK inhibitor that blocks JAK1 and 2

A

Baricitinib

47
Q

this is a JAK inhibitor that blocks JAK1 and 3

A

tofacitinib

48
Q

_________ focus is on methods of action in the cytokine cascade. they reduce signs/symptoms of RA and inhibit. structural damage in patients with moderate.severe to severe RA. they are often given i.v. or sc and either along or in combination with methotrexate for better disease control

A

biologic response modifiers

49
Q

________ either “sponge the excess TNF (Etanercept), prevent cell surface and soluble TNF binding to its receptor (infliximab), or bind directly to TNF, blocking TNF receptors (Adalimumab)

A

TNF inhibitors

50
Q

_______ selectively inhibits T cells (similar to CTLA4)

A

Abatacept

51
Q

________ was originally developed and used for B cell non-Hodgkins Lymphoma and is an anti-CD20 monoclonal antibody

A

Rituximab

52
Q

this is an immunosuppressant agent that may be used in RA. the exact MOA is not understood. it used used in patients that have not responded to other medications or in combination therapy

A

azathioprine (Imuran, Azasan)

53
Q

this is an immunosuppressant agent that may be used in RA. it primarily affects T cell signalling

A

cyclosporine (Gengraf, Neoral, Sandimmune)

54
Q

true or false: treatment with single non-biological DMARDs can achieve remission

A

true

55
Q

when are combinations of non-biological DMARDs indicated?

A

for patients with moderate or high disease activity or prolonged disease duration or for those who fail to respond to a single compound

56
Q

_________ are reserved for patient with persistent moderate ro high disease activity and indicators of poor prognosis

A

biologic DMARDs

57
Q

__________ are often used to bing the level of inflammation quickly under control

A

short term glucocorticoids

58
Q

why are glucocorticoids not suitable for long term use

A

due to adrenal suppression and severe side effects

59
Q

this is characterized biochemically by hyperuricemia and clinically by episodes of severe, acute arthritis. acute attacks occur as a result of an inflammatory reaction to crystals of uric acid that are deposited in the joint

A

gout

60
Q

explain uric acid metabolism

A

xanthine oxidase breaks down hypoxanthine to xanthine to the keto form of uric acid and finally to the enrol form of uric acid

61
Q

explain the MOA of allopurinol

A

this is an analog of hypoxanthine, therefore is serves as a substrate for the enzyme xanthine oxidase and further stops the production of uric acid.

62
Q

is allopurinol used to treat acute gout attacks or used for prophylaxis

A

prophylaxis

63
Q

is allopurinol absorbed well?

A

rapid oral absorption

64
Q

is allopurinol bound to plasma proteins

A

no

65
Q

where does allopurinol distribute

A

in total body water (2/3 less in brain)

66
Q

what are some side effects of allopurinol

A

GI irration -> diarrhea

67
Q

this gout agent is an antibiotic: it interferes with mitotic spindles and arrests cells in metaphase. it causes depolymerization and disappearance of fibrillar microtubules in granulocytes and other motile cells. decreases intracellular translocation involved in histamine release therefore less inflammation

A

colchicine

68
Q

is colchicine used to treat acute gout or prophylaxis

A

acute

69
Q

is colchicine absorbed well?

A

rapid oral absorption (peak plasma concentration in 30min - 2hrs)

70
Q

where is colchicine distributed in the body

A

high concentration in liver, spleen and kidneys; excluded from heart, muscle and brain

71
Q

how is colchicine excreted

A

fecal excretion of metabolites

72
Q

which population is colchicine less tolerated in

A

elderly

73
Q

what are some side effects of colchicine

A
  • GI (N/V/D)
  • acute poisoning (GI hemorrhage, vascular damage, CNS paralysis)
  • chronic poisoning (bone marrow effects)
74
Q

this is a uricosuric agent used to treat gout. it blocks the reabsorption of uric acid, therefore it leaves the body instead of building up

A

Probenecid (Benemid)

75
Q

this is a uricosuric agent used to treat gout. it inhibits uric acid reabsorption in the proximal tubule of the kidney

A

Sulfinpyrazone (Anturane)

76
Q

what is the MOA of uricosuric agents

A

inhibition of the URAT1 (anion exchanger) in the kidneys and thus blocking reabsorption

77
Q

this is another agent that may be used for gout. includes indomethacin or naproxen

A

NSAIDs

78
Q

this is another agent that may be used for gout. it inhibits xanthine oxidase

A

Febuxostat

79
Q

this is another agent that may be used for gout. it is an anti-hyperlipidemic drug that is most commonly used in combination with allopurinol

A

fenofibrate

80
Q

this is another agent that may be used for gout. is is an angiotensin II receptor antagonist. it also blocks uric acid reabsorption. usually used to treat gout in patients who have hypertensions

A

losartan

81
Q

this is another agent that may be used for gout. 4g of ascorbic acid daily nearly doubles the fractional excretion of uric acid

A

vitamin C

pharmacology 4810 (12 decks)

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