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Pathopharm II Exam 1 > 2: RA/Gout/Movement (Part 1) > Flashcards

2: RA/Gout/Movement (Part 1) Flashcards

1
Q

DMARDs were formerly considered….

Disease-modifying antirheumatic drugs

A

toxic drugs

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2
Q

only symptomatic treatment for RA

A

NSAIDS

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3
Q

what is function of DMARDS

A

Some may slow progression of RA; effects not seen for weeks or months, i.e., slow-acting.

Different mechanism than NSAIDS.

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4
Q

what can gold be used for

A

anti-rheumatic

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5
Q

gold mechanism of action

A

unknown

  • may alter macrophage function & morphology
  • selectively accumulate in macrophages in the inflamed synovium
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6
Q

plasma half life of Gold

A

7 days

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7
Q

gold tissue binding

A

avidly binds to tissues (found in liver and skin several years after therapy is DC’d

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8
Q

how is gold excreted

A

urine and feces

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9
Q

what gold salt is available as parenteral preparation for IM administration

A

gold sodium thiomalate (Myochrysine) – not in US, but available in Canada

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10
Q

orally effective gold preparation

A

auranofin (ridaura)

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11
Q

most common side effect with gold

A

dermatitis (pruritus reaction is warning signal)

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12
Q

what reactions are also common with gold use

A

mucous membrane reactions

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13
Q

what other effects are observed with the use of Gold

A

Stomatitis and ulcers on buccal membranes and tongue are observed.

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14
Q

skin toxicities with gold cause…

A

a bluish-gray pigmentation (chrysiasis); effects are seen in 15-20% of patients.

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15
Q

serious toxicities of gold use include (2)

A

bone marrow depression (blood counts mandatory)

renal reactions such as nephrotic syndrome.

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16
Q

what gold is better tolerated but causes a higher incidence of GI disturbances

A

auranofin

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17
Q

hydroxychloroquine mechanism of action

A

Unknown, but effects may be, in part, to stabilize lysosomal membranes.

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18
Q

use of hydroxychloroquine used as an anti-inflammatory agent requires…

A

large doses for long periods of time.

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19
Q

hydroxychloroquine may cause what ocular effects

A

cause serious damage to the retina where the drug is preferentially concentrated

The retinal damage may be irreversible and may progress after the drug is discontinued.

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20
Q

what other effects can hydroxychloroquine cause

A

dermatitis, ototoxicity, and neuromyopathy.

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21
Q

what kind of medication is D-Penicillamine (Cuprimine)

A

chelator

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22
Q

mechanism of action of D-Penicillamine

A

unknown, but may affect immune system.

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23
Q

how does D-Penicillamine work

A

dermatitis, ototoxicity, and neuromyopathy.

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24
Q

side effects with use of D-penicillamine

A
  • loss of taste perception
  • nephrotoxicity
  • myasthenia-like syndrome
  • rash
  • thrombocytopenia and leukopenia
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25
Q

what kind of drugs are azathioprine and methotraxate

A

cytotoxic agents

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26
Q

cytotoxic drugs mechanism of action

A

possible direct anti-inflammatory + suppress/modify immune responses

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27
Q

what are the very serious side effects that can be caused by azathioprine and methotrexate

A

bone marrow depression, sterility, and carcinogenic and mutagenic effects.

***In spite of these effects, aggressive early treatment with methotrexate can prevent major manifestations of RA before irreversible damage becomes prevalent.

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28
Q

Recent clinical studies have shown that of all of DMARDS, ____________ has the best benefit-to-risk ratio.

A

methotrexate

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29
Q

how is methotrexate used

A

ONCE A WEEK in very small doses (“low-dose pulse therapy”).

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30
Q

mucosal ulcers are common with?

A

methotrexate use once a week in very small doses

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31
Q

function of TNF blockers

A

Proteins that block TNF (Tumor Necrosis Factor) which is a large group of cytokines, at it’s receptor

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32
Q

TNF is responsible for…

A

triggering immune response and is present in larger amounts in patients with RA and some other immune disorders such as ankylosing spondylitis and psoriasis.

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33
Q

TNF increases

A

body inflammatory reaction

34
Q

increased risk of infections with TNF blockers is due to

A

inhibited immune function

35
Q

side effects of TNF blockers

A
  • occasional fatal blood dyscrasias
  • nervous system disorders
  • seizures
  • increased risk of some cancers (ie lymphoma).
36
Q

JAK1, JAK2, JAK3 are enzymes that

A

play a part in the signaling pathways started by cytokines at their receptors

37
Q

inhibition of JAK enzymes block….

A

cytokine signaling

and can decrease various immune and inflammatory responses

38
Q

a JAK1/JAK2 inhibitor for RA

A

Ruxolitinib (Jakafi)

39
Q

a JAK1/JAK2 inhibitor for RA

A

Baricitinib (Olumiant)

40
Q

JAK3 inhibitor for moderate to severe RA not responding to methotrexate

A

Tofacitinib (Xeljanz)

41
Q

gout pathophysiology

A
  • chronic disease
  • biochemically: a disorder of uric acid metabolism
  • clincially: hyperuricemia & recurrent attacks of acute arthritis caused by deposition of crystals of sodium urate in tissues, especially joints and the kidney.
42
Q

____________ is the end product of purine metabolism and is poorly soluble, especially in acid environments.

A

uric acid

43
Q

where is gout usually found

A

joint of the big toe

44
Q

what does deposition of crystals of sodium urate in the tissues, joints and kidneys cause

A

acute inflammatory reactions, and tophi or inflamed swellings

45
Q

When blood uric acid level becomes saturated…

A

neutrophils phagocytize the crystals.

46
Q

when crystals are phagocytized by neutrophils, they fuse with…

A

lysosomes

47
Q

lysosomes eventually rupture and cause the cell to lyse, releasing

A

lysosomal enzymes and inflammatory and chemotactic mediators such as PGs, IL-1, and lactate (which decreases pH, so solubility of urate decreases - vicious cycle!).

48
Q

PGs, IL-1, and lactate attract….

A

PMNs (polymorphonuclear neutrophils) to the site.

49
Q

causes for both hyperuricemia and acute arthritic episodes

A
  • drug effects
  • renal damage
  • metabolic
  • increased nucleic acid turnover
  • enzyme defect
  • local decrease in urate solubility
  • increased urate production
50
Q

drug therapy for gout
2 primary aims

A

prevent/reduce the inflammation & pain of the acute attack

reduce blood urate levels (<6 mg/dl); increase urate excretion or decrease production.

51
Q

dietary changes for gout

A

reduce amount of purines in diet

52
Q

non pharm treatment for gout

A

dietary changes
weight reduction
adequate fluid intake
limit ETOH consumption

53
Q

Drugs that Increase Urate Excretion (uricosurics):

A

Probenecid

54
Q

Drugs that Decrease Uric Acid Production:

A

Allopurinol (Zyloprim)

Febuxostat (Uloric)

55
Q

what drug is an alkaloid of Colchicum autumnale (autumn crocus, meadow saffron)

A

Colchicine

56
Q

mechanism of action of colchicine

A
  • Binds to tubulin & disrupts mitotic spindles
  • causes depolymerization
  • affects microtubules in granulocytes & inflammatory cells; cannot migrate to the inflamed area
57
Q

the net effect of colchicine in gout attacks

A

is to decrease release of lactic acid

58
Q

colchicine uses

A

Effective at the onset of symptoms and gives prompt relief

59
Q

How fast does colchicine reduces symptoms of gout?

A

within 12 hours (pain, swelling, redness)

symptoms completely gone within 48-72 hrs

60
Q

colchicine is also useful as…

A

a prophylactic agent in very low doses at the initiation of treatment with other anti-gout drugs to decrease risk of acute attacks of gout (0.5 mg 2-4 times/wk).

61
Q

what happens with colchicine causing the cessation of mitotic spindle formation

A
  • mitosis is arrested at metaphase
  • affects cells with high division rates (rapidly proliferating cells of the GI tract)
62
Q

GI symptoms with colchicine

A

nausea, vomiting, abdominal pain, and diarrhea in 80%

63
Q

a serious symptom of colchicine OD

A

hemorrhagic gastroenteritis

64
Q

if colchicine is not stopped after patient experiences hemorrhagic gastroenteritis what may occur

A

can progress to vascular damage, renal toxicity, muscular depression (kills muscle cells), and paralysis (CNS mediated).

65
Q

how is colchicine administered

A
  • PO (pushing the dose until pain relief or diarrhea)
  • IV (works faster and can avoid GI side effects)
66
Q

extravasation with colchicine can cause

A

severe tissue necrosis

67
Q

Although colchicine can arrest cell division, effects on ____________ , etc. are not common problems with usual therapeutic doses (but may be seen with long term use).

A

bone marrow, gonads

68
Q

colchicine can be used with what other drugs

A

probenecid and allopurinol.

69
Q

____________ is marketed in several combination products with probenecid.

A

colchicine

70
Q

NSAID of choice in acute gout attack

A

indomethacin

71
Q

with NSAIDS, the inhibition of ____________ by these drugs accounts for many of their clinical effects on inflammation and pain

A

prostaglandin synthesis

72
Q

steroid use in acute gout attacks

A

these drugs accounts for many of their clinical effects on inflammation and pain

73
Q

probenecid mechanism of action

A

blocks reabsorption of urate in the renal proximal tubule.

Also blocks urate secretion, but effects on reabsorption predominate and the net result is increased urate excretion in urine - a uricosuric effect.

Uricosuric

74
Q

____________ is the prototype inhibitor of organic anion secretion (used to increase t1/2 of penicillin by decreasing its secretion).

A

probenecid

75
Q

when used in sufficient amounts, ____________ interferes with uric acid reabsorption.

A

probenecid

76
Q

when using probenecid with uricosuric agents, there is a ____________ effect

A

paradoxical

77
Q

paradoxical effect of using probenecid with uricosuric agents

A

small doses can compete with uric acid for tubular secretion and occasionally may even increase serum uric acid concentration.

78
Q

initiation of probenecid therapy may precipitate…

A

an acute gout attack

79
Q

prophylactic use of ____________ can prevent the acute attack

A

colchicine or an NSAID

80
Q

It is best not to start treatment with a uricosuric until ____________ after an acute gout attack.

A

1-2 weeks

81
Q
A

Pathopharm II Exam 1 (11 decks)

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