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Pharmacology for APRN > OA, Gout, Osteoporosis > Flashcards

OA, Gout, Osteoporosis Flashcards

1
Q

Osteoarthritis Defined

A

Progressive disease can result in chronic pain, restricted ROM, and muscle weakness, especially if a weight-bearing joint such as knees, hips, cervical or lumbar spine, distal interphalangeal (DIP) joints, and carpometacarpal joint (base of the thumb) is affected.

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2
Q

Osteoarthritis Forms Defined

A

Primary or Idiopathic: Arises from physiologic changes that occur with normal aging
Secondary: results from traumatic injuries or inherited conditions and may present as hemochromatosis, chondrodystrophy, or inflammatory OA.

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3
Q

Osteoarthritis Pathophysiology

A

OA must be differentiated from other forms of arthritis because the physiologic changes specific to the condition dictate disease management.
Although most forms of arthritis, including OA, result in degeneration of articular cartilage, the subsequent formation of new bone is a change specific to OA.

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4
Q

Osteoarthritis Diagnostic Criteria: Hand

A

Pain, aching, or stiffness and three of the following:
Hard tissue enlargement of >2 joints; Hard tissue enlargement of >2 DIP joints; <3 swollen metacarpophalangeal joints; deformity of >1 selected joint

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5
Q

Osteoarthritis Diagnostic Criteria: Hip

A

Pain and two of the following:
Erythrocyte sedimentation rate (ESR) <20 mm/h; Radiographic femoral or acetabular osteophytes; Radiographic joint space narrowing

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6
Q

Osteoarthritis Diagnostic Criteria: Knee

A

Knee pain and three of the following:
>50-year-old; stiffness <30 minutes; crepitus; bony tenderness, Bony enlargement; no palpable warmth

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7
Q

OA Diagnostic Criteria: Clinical and Radiographic Diagnosis

A

Knee pain and osteophytes and one of the following:
>50-year-old; stiffness <30 minutes; crepitus

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8
Q

OA Diagnostic Criteria: Clinical and Laboratory diagnosis

A

Knee pain and 5 of the following:
Age >50 years; stiffness <30 minutes; crepitus; bony tenderness; bony enlargement; no palpable warmth; ESR <40 mm/h; RF <1:40; synovial fluid signs of OA (clear, viscous, or WBC count <2,000/mm3)

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9
Q

OA Topical NSAID’s Indications

A

Topical therapy is preferred over systemic therapy by the European League Against Rheumatism (EULAR) and the Osteoarthritis Research Society International (OARSI).
Topical nonsteroidal antiinflammatory drugs (NSAIDs) are strongly recommended by the American College of Rheumatology (ACR) for knee osteoarthritis and conditionally for hand osteoarthritis. Due to concerns with absorption in hip osteoarthritis, topical therapy is typically not recommended.
Systemic therapy may be more effective depending on the number and location of joints affected. Topical therapy is an attractive option due to the relatively benign side effect profiles.

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10
Q

OA NSAID Indications

A

2nd line therapy = oral NSAIDs
NSAIDs further classified according to their chemical structure, all exhibit cyclooxygenase (COX) inhibition.

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11
Q

A practitioner is prescribing a medication for a patient recently diagnosed with OA. What is the recommended first line of treatment for OA?

A

Acetaminophen. First-line pharmacotherapy for OA is geared toward analgesia, specifically with acetaminophen (Tylenol). Due to acetaminophen’s cost effectiveness and safety, it is currently the first-line treatment recommended in guidelines by the ACR, the EULAR, and others.

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12
Q

Diclofenac (Voltaren) MOA

A

The mechanism of action for topical diclofenac is the same as for oral
NSAIDs. The benefit is that minimal diclofenac is absorbed when applied topically, which then
decreases the risk of adverse events. Data have shown that only 6% to 10% of the topical gel and
2% to 3% of the solution is absorbed.

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13
Q

Diclofenac (Voltaren) Dosage

A

LE’s: 4 g should be applied four times a day; if used on the UE’s: 2 g should be applied four times a day. The entire total daily dose should not exceed
32 g/d.

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14
Q

Diclofenac (Voltaren) Contraindications

A

Topical diclofenac carries the same warnings and contraindications as oral
NSAIDs, although the risk is less. Also, topical diclofenac is contraindicated on non-intact or
damaged skin.

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15
Q

Diclofenac (Voltaren) Adverse Events

A

pruritus, rash, dry skin, pain, and exfoliation.

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16
Q

Capsaicin MOA

A

Depletes substance P.
Initially, capsaicin releases substance P from the peripheral sensory
neurons.
With time, substance P becomes depleted, and capsaicin prevents
reaccumulation of substance P.

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17
Q

What is Substance P?

A

Substance P is a chemomediator responsible for pain
transmission from the periphery to the central nervous system (CNS).

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18
Q

Capsaicin Dose

A

Capsaicin is available as an over-the-counter (OTC) product in a patch, cream, gel,
liquid, or lotion.
Effect seen after 2-4 weeks of use

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19
Q

Capsaicin Contraindications, Adverse Events

A

Contraindication: None.
SE: burning and irritation at the application
site.

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20
Q

Oral NSAID MOA

A

One is by
inhibiting the conversion of arachidonic acid to prostaglandin, prostacyclin, and thromboxanes—
all of which are mediators of pain and inflammation. The other is by interfering with protein
kinase activation (especially when taken at higher doses).
Most non-selectively inhibit COX-1 and COX-2

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21
Q

What is COX?

A

The enzyme that converts arachidonic acid to prostaglandin G2.

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22
Q

What does COX-1 do?

A

COX-1 enzymes are found in
the gastrointestinal (GI) tract and kidney and produce protective prostaglandins,

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23
Q

What does COX-2 do?

A

COX-2 produces protective prostaglandins in
the kidney that are responsible for maintaining adequate blood perfusion via vasodilation of the
afferent arteriole.
Inhibition of COX-2 produces antiinflammatory
and analgesic effects without affecting the GI tract.

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24
Q

NSAID Contraindications

A

Pregnant women
Caution with liver or kidney disease
Aspirin allergy
EtOH dependence
all NSAIDs carry a black box warning emphasizing that they are contraindicated for
perioperative pain treatment in patients undergoing coronary artery bypass graft surgery and
should be avoided in patients with cardiovascular disease or risk factors.

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25
Q

What is a COX-2 selective NSAID?

A

Celecoxib (Celebrex)

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26
Q

Nonacetylated Salicylates Use

A

For those who are sensitive to the GI irritation caused by long-term ASA use

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27
Q

Diflunisal (Dolobid) Nonacetylated Salicylate MOA

A

Effective COX-1 inhibitor with antiinflammatory and analgesic properties, but its antipyretic activities are weak.

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28
Q

Acetaminophen (Tylenol) Indications

A

For patients with limited pharmacologic options due to intolerance or contraindications to the use of NSAIDs
Best for short term use
Risk of hepatotoxicity

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29
Q

Acetaminophen (Tylenol) MOA

A

Acetaminophen exerts its action within the CNS. It is thought to inhibit central COX, which
results in decreased prostaglandin synthesis. Through this prostaglandin inhibition,
acetaminophen exerts analgesic and antipyretic effects but does not have antiinflammatory
effects.

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30
Q

Analgesics in OA Indications

A

When the pain associated with OA progresses and is no longer responsive to acetaminophen or NSAIDs, analgesics are an option.
For those who have contraindication to NSAID or cannot tolerate them

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31
Q

Acetaminophen (Tylenol) Drug Interactions

A

Warfarin.
With chronic doses of greater than 1.3 g daily, acetaminophen can increase the international
normalized ratio (INR) of a patient on warfarin.

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32
Q

Tramadol (Ultram = extended release, Ultracet = tylenol combo) MOA

A

Tramadol exerts multiple effects to induce pain relief. It is a mu-opioid
receptor agonist similar to other opioids such as morphine. By binding to the mu-opioid receptor,
ascending pain pathways are inhibited, resulting in decreased pain sensation. In addition,
tramadol also inhibits the reuptake of serotonin and norepinephrine. These neurotransmitters are also involved in the ascending pain pathway.

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33
Q

Tramadol Contraindications

A

Sz d/o - lowers Sz threshold
EtOH dependence - CNS effects
Opioid Dependence - acts on opioid receptors

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34
Q

Tramadol Interactions

A

Tramadol is metabolized by CYP2D6, and any medication that inhibits or induces
this enzyme will interact with tramadol.
Inhibits serotonin reuptake, tramadol
has the potential to induce serotonin syndrome when used in combination with other serotonergic
agents, such as selective serotonin reuptake inhibitors, tricyclic antidepressants, monoamine
oxidase inhibitors, or linezolid.

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35
Q

Duloxetine MOA

A

Duloxetine is a serotonin and norepinephrine reuptake inhibitor. By enhancing serotonin and norepinephrine, duloxetine works in the CNS to reduce pain transmission.

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36
Q

Duloxetine Dosing

A

Food and Drug Administration (FDA) for chronic
musculoskeletal pain is 30 mg orally daily for 7 days and then increased to 60 mg orally daily,

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37
Q

Duloxetine Contraindications

A

Due to the risk for serotonin syndrome, duloxetine should not be started
while a patient is on a monoamine oxidase inhibitor (MAOI) or within 14 days of stopping an
MAOI.
If current linezolid IV therapy or methylene blue IV therapy

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38
Q

Duloxetine Adverse Effects

A

precautions and warnings associated with duloxetine risk include
hepatotoxicity, orthostatic hypotension, serotonin syndrome, abnormal bleeding, and activation
of mania.

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39
Q

Intra-articular Therapy for OA: Indications

A

If symptoms of OA are restricted to one or two joints that have not responded to first- or second-line treatment, intra-articular corticosteroids may be helpful.

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40
Q

First-Line Therapy for OA

A

The EULAR
continues to recommend acetaminophen as first-line therapy for hip and knee OA (last updated
in 2005 and 2003 respectively). Due to questionable efficacy and risk for hepatotoxicity, more
recent guidelines recommend topical therapies as first line

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41
Q

Second-Line Therapy for OA

A

Oral Non-selective NSAIDs
COX-2 inhibitor for those with GI issues

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42
Q

Gout Definition

A

Gout is an inflammatory condition that results from monosodium urate crystals precipitating in the synovial fluid between joints due to hyperuricemia.

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43
Q

Gout Pathophysiology

A

The monosodium urate crystals form due to hyperuricemia either from overproduction or from under-excretion of uric acid.

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44
Q

Gout Commonly affected Joints

A

Most Common: metatarsophalangeal joint.
Midtarsal joints, ankles, knees, fingers, wrists, and elbows.

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45
Q

Gout Diagnostic Criteria

A

Diagnosis of gout usually occurs clinically when a patient is experiencing rapid monoarticular arthritis, typically in the first metatarsophalangeal joint. This arthritis is accompanied by swelling and redness of the joint.

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46
Q

Xanthine Oxidase Inhibitors (Allopurinol, Febuxostat) for Chronic Gout MOA

A

XOIs decrease uric acid levels by selectively inhibiting xanthine oxidase.
Xanthine oxidase is the enzyme responsible for the conversion of hypoxanthine to xanthine to
uric acid. Hypoxanthine and xanthine are then excreted in the urine with little risk of
precipitation.

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47
Q

XOIs Adverse Events

A

Rash,
arthralgias, and GI complications, which can be reduced by taking the medication with food.
Allopurinol: need to renal adjust dose!

48
Q

Goal of Gout Treatment - Chronic

A

The goals of drug therapy in chronic gout are to decrease the serum urate level to less than 6 mg/dL and to decrease the occurrence of acute gout attacks.
To prevent gout flares, patients should take NSAIDs or colchicine for the first 6 months of urate-lowering therapy.

49
Q

Goal of Gout Treatment - Acute

A

For an acute gout attack, the goals are to relieve pain, terminate the attack, and maintain joint function.
When an acute gout attack occurs, patients can rest the joint and apply ice as needed to help with pain. They can also use short courses of NSAIDs, corticosteroids, or colchicine to reduce pain.

50
Q

Uricosuric Agent (Probenecid) Indications

A

The 2012 update to the ACR guidelines also recommends the addition of probenecid to a XOI if serum uric acid levels are not at goal with a XOI alone.

51
Q

Probenecid MOA

A

Probenecid increases the excretion of serum uric acid by inhibiting
transporter proteins responsible for the reabsorption of uric acid in the kidneys.

52
Q

Probenecid Contraindications

A

Probenecid should not be given during an acute gout attack as it could exacerbate the symptoms when initiated.
Children <2 yrs old.

53
Q

Probenecid Adverse Events

A

Serious
reactions that can occur include hemolytic anemia and aplastic anemia in patients with G6PD
deficiency, hepatic necrosis, and anaphylaxis.

54
Q

Last-line Gout Therapy: Pegloticase MOA

A

Pegloticase is a pegylated recombinant form of uricase. Uricase is an
enzyme typically absent in humans but is found in high levels in primates. Uricase converts uric
acid to allantoin, which is an inactive, water-soluble metabolite of uric acid allowing uric acid to
be easily excreted by the kidneys.

55
Q

Pegloticase Considerations

A

It must be administered intravenously in a health care facility every 2 weeks and costs more than $5,000 per dose.

56
Q

Colchicine for Acute Gout: MOA

A

Colchicine inhibits the activation, degranulation, and migration of
neutrophils to the area of a gout attack. This then decreases the inflammation and pain associated
with a gout attack.

57
Q

Osteoporosis Definition

A

Osteoporosis is a progressive systemic disease characterized by a decrease in bone mass and microarchitectural deterioration of bone tissue, resulting in bone fragility and increased susceptibility to fractures.

58
Q

Common sites of Osteoporosis Fx

A

Vertebral Compression Fx
Fx of Distal Radius
Fx of the Proximal Femur

59
Q

Type I: Postmenopausal Osteoporosis Definition

A

Postmenopausal women between ages 51 and 75.
Decreased estrogen causes an accelerated rate of bone loss, especially trabecular bone loss.
Fx at site of Vertebrae and distal femur, tooth loss common.

60
Q

Type II: Senile Osteoporosis Definition

A

Men & Women >70yrs old
Proportional loss of cortical and trabecular bone
Most common Fx to hip, pelvis, and vertebrae

61
Q

Type III: Secondary Osteoporosis Definition

A

Men and Women of any age
Secondary to other conditions such as drug therapy or other diseases

62
Q

For which patient would a diagnosis of type III osteoporosis be considered?
A. A postmenopausal woman who fractures a femur
B. A 75-year-old man who breaks a hip
C. A 45-year-old woman who takes medicine for hyperparathyroidism
D. A 60-year-old woman who is experiencing tooth loss

A

“C”
Type III: secondary osteoporosis occurs in men and women of any age and is secondary to other conditions such as drug therapy and other disease. A 75-year-old man who breaks a hip may have type II: senile osteoporosis. A postmenopausal woman experiencing fractures and tooth loss may have type I: postmenopausal osteoporosis.

63
Q

Osteoporosis Risk Factors

A

Female Sex, older age, Asian or White descent
Family History, petite stature, low body weight
Amenorrhea, Menopause
Sedentary lifestyle, low calcium intake
Excess alcohol intake, smoking, excess caffeine intake
Low testosterone in men
Certain drugs/disease states

64
Q

Diagnostic Tools for Osteoporosis

A

FRAX: Ten risk factors considered in addition to the bone mineral density (BMD) T-score: age, gender, fracture history, parental hip fracture history, oral steroid therapy, low body mass index, femoral neck BMD, secondary osteoporosis, current smoking, and alcohol intake.
WHO Fx Risk Assessment Tool

65
Q

T-Score for Osteoporosis Diagnosis

A

The T-
score compares a person’s measured BMD to the average peak BMD of a healthy, young white
adult of the same sex.
A normal T-score is ≥ -1, whereas osteopenia (low bone mass) is diagnosed with a T-score of
-1 to -2.4.

66
Q

Indications for Drug Therapy for Osteoporosis

A
  1. A hip or vertebral (clinical or morphometric) fracture
  2. (T-score from -1.0 to -2.5 at the femoral neck, total hip, or spine) and a 10-
    year probability of hip fracture of ≥3% or more or a 10-year probability of any major
    osteoporosis-related fracture of ≥20%
  3. T-score ≤ -2.5 at the femoral neck, total hip, or spine by DEXA scan
67
Q

What are the goals of Osteoporosis drug therapy?

A

Minimizing bone loss
Delaying the progression of osteoporosis
Preventing fractures and fracture-related morbidity and mortality

68
Q

Alendronate (Fosamax) Bisphosphonate Class Drug Treatement

A

Prevention: 5 mg/d or 35 mg once a week; treatment: 10 mg/d or 70 mg once a week

69
Q

Bisphosphonate Treatment for Osteoporosis: MOA

A

These drugs inhibit bone resorption and increase bone density. They are deposited in the bone at
sites of mineralization and in resorption lacunae. The bone resorption and fracture rates decline,
whereas bone density increases.

70
Q

Risedronate (Actonel) Bisphosphonate Class Drug Treatment for Osteoporosis

A

5 mg/d or 35 mg once a week

71
Q

Ibandronate (Boniva): Bisphosphonate Class Drug Treatment for Osteoporosis

A

2.5 mg PO QD or 150 mg PO once a month or 3 mg/3 mL IV every 3 months

72
Q

Zoledronic Acid (Reclast): Bisphosphonate Class Drug Treatment for Osteoporosis

A

5 mg/100 mL once daily

73
Q

Bisphosphonate Patient Education

A

PO is poorly absorbed, take at the same time every day or same time every month depending on dosing. Take with food and water. Stay upright 30min after taking.

74
Q

Bisphosphate Adverse Events

A

Esophagitis
Contraindicated if CrCl <35
Osteonecrosis of the jaw with long-term use
Atypical femur Fx with long-term use

75
Q

Selective Estrogen Receptor Modulator: Raloxifene (Evista) for Osteoporosis prevention MOA

A

SERMs mimic the effects of estrogen on bones without replicating the stimulating effects of
estrogen on the breasts and uterus. They decrease bone resorption and bone turnover.
60mg QD

76
Q

PTH Modifiers: Teriparatide (Forteo) & Abaloparatide (Tymlos) for Osteoporosis Prevention MOA

A

PTH is the primary regulator of calcium and phosphate metabolism and regulates bone
metabolism, renal tubular reabsorption of calcium and phosphates, and intestinal calcium
absorption. It stimulates new bone formation in trabecular and cortical bone surface by preferential stimulation of osteoblastic activity over osteoclastic activity.

77
Q

Teriparatide (Forteo) & Abaloparatide (Tymlos) for Osteoporosis Prevention Contraindications

A

Patients with
Paget’s disease, children, and patients with previous bone radiation therapy, a history of skeletal
malignancy (increased risk of osteosarcoma in rat studies), metabolic bone disease,
hypercalcemia (which is usually transient), and hyperparathyroidism

78
Q

RANK Ligand Inhibitor: Denosumab (Prolia) for Osteoporosis Prevention and treatment MOA

A

In postmenopausal osteoporosis, decreased estrogen leads to increased RANK ligand, an
essential mediator of osteoclast activity. Denosumab is a monoclonal antibody that binds to the
RANK ligand and blocks its interaction with RANK to prevent osteoclast formation (which
increases bone loss and fracture risk), thus preventing bone resorption.
60mg SQ q 6mon

79
Q

A practitioner is prescribing Fosamax for a patient with osteoporosis. What is the recommended dosage for treatment?
A. 10 mg/d
B. 5 mg/d
C. 2.5 mg/d
D. 60 mg QD

A

A. 10 mg/d

Rationale: The bisphosphonate alendronate (Fosamax) is dosed; Prevention: 5 mg/d or 35 mg once a week; and Treatment: 10 mg/d or 70 mg once a week.

80
Q

First line Prevention and Treatment for Osteoporosis

A

Prevention: raloxifene, alendronate, ibandronate, zoledronic acid, or risedronate plus calcium and vitamin D
Treatment: raloxifene, alendronate, risedronate, ibandronate, zoledronic acid, or calcitonin

81
Q

Second Line Prevention and Treatment for Osteoporosis

A

Same as first line.
Addition of hormone modifiers or calcitonin if not being taken

82
Q

A practitioner is prescribing a second-line treatment for a patient whose osteoporosis is not responding to the first line. What drug would be added?
A. Raloxifene
B. Alendronate
C. Zoledronic acid
D. Hormone modifier

A

D. Hormone modifier

Rationale: The first line of treatment is raloxifene, alendronate, risedronate, ibandronate, zoledronic acid, or calcitonin. The second line of treatment is to add a hormone modifier or calcitonin if not being taken.

83
Q

RA Definition

A

Chronic autoimmune inflammatory disease characterized by symmetric polyarthritis and joint changes, including erythema, effusion, and tenderness.
The course of rheumatoid arthritis (RA) is characterized by remissions and exacerbations.
RA can affect several organs, but it usually involves synovial tissue changes in the freely movable joints (diarthroses).

84
Q

RA Causes

A

Genetic factors
Infectious agents
Environmental factors
An antigen–antibody response

85
Q

RA Pathophysiology

A

Synovial membrane proliferation
followed by erosion of the subarticular cartilage and subchondral bone. Although the precise
etiology of RA is unknown, mounting evidence points to a series of immunologic events. It is unclear whether an infectious, viral, or genetic agent prompts these events.

86
Q

Early Phase RA Characteristics

A

the synovium becomes more vascularized, and proliferation and

hypertrophy begin. This results in the synovial tissue becoming edematous and exhibiting frond-
like villi. As leukocytes proliferate, the synovial fluid becomes less viscous.

87
Q

RA Progression Characteristics

A

Continued hyperplasia and hypertrophy of the synovial lining occur.
The thickness of the synovial lining increases up to fivefold from the normal one or two cell layers.
The proliferation of the synovium persists, with lymphocytic tissue and plasma cells forming around blood vessels.
This proliferative tissue extends into the joint space, joint capsule, ligaments, and tendons.

88
Q

What is “Pannus” in RA and why is it specific to RA?

A

Pannus is granulation tissue composed of lymphocytes, plasma cells, fibroblasts, and macrophages.
Pannus begins at synovium and extends to the junction of cartilage and subchondral bone.
Pannus erodes into surrounding tissue, tendons, and cartilage.
Pannus causes decreased ROM and ankylosis may ensue.

89
Q

Goals of Drug Therapy in the treatment of RA

A

Reducing pain, stiffness, and swelling
Preserving mobility and joint function
Preventing further joint damage

90
Q

What drug is a mainstay in the treatment of RA?

A

NSAIDs: used to help relieve immediate pain and improve symptoms during the diagnostic process.

91
Q

Diagnostic Criteria used for RA - tool is scored positive for RA if score >6

A

Joint Involvement (Scores 1-greater than 10 joints)
Serology Findings (Measures RF and ACPA)
Acute Phase Reactants (measures ESR & CRP)
Duration of Symptoms (on a scale of less than or greater than 6mon)

92
Q

Disease-Modifying Antirheumatic Drug (DMARD) List

A

Methotrexate
Sulfasalazine
Antimalarials
Leflunomide
Initiate within 3mon after the onset of symptoms!

93
Q

Corticosteroids in RA treatment

A

Low-dose corticosteroids (<prednisone 10 mg or equivalent) are beneficial in patients who are beginning DMARD therapy.
Because the therapeutic effect of DMARDs may not be seen until several weeks to months after initiating therapy, corticosteroids may be used to provide almost immediate symptom relief and bridge patients until DMARDs take effect.

94
Q

A practitioner is prescribing Humira for a patient with RA. What is the recommended dosage?
A. 50 mg SQ monthly in combination with methotrexate
B. 400 mg SQ at weeks 0, 2, and 4 and then 200 mg every other week
C. 100 mg SQ daily
D. 40 mg SQ every other week

A

D. 40 mg SQ every other week

Rationale: The recommended dosage for Humira is 40 mg SQ every other week; 40 mg weekly as monotherapy. The dosage for Simponi is 50 mg SQ monthly in combination with methotrexate, for Cimzia is 400 mg SQ at weeks 0, 2, and 4 then 200 mg every other week, and for Kineret is 100 mg SQ daily.

95
Q

A practitioner is prescribing an agent for a patient with RA who failed phase I treatment. What would be the recommended therapy?
A. Methotrexate monotherapy
B. Leflunomide
C. Sulfasalazine
D. bDMARD

A

D. bDMARD

Rationale: Upon failure of phase I, with poor prognostic factors: bDMARD is recommended, without poor prognositic factors changing csDMARDs is recommended. Treatment for phase I is methotrexate monotherapy or combination; if contraindication to methotrexate: leflunomide or sulfasalazine alone or combination.

96
Q

Methotrexate (DMARD) MOA

A

Methotrexate, a folic acid antagonist, is thought to affect leukocyte suppression, decreasing the
inflammation that results from immunologic by-products.

97
Q

Methotrexate (DMARD) Dosing Considerations

A

7.5 mg orally once per week is recommended. If a significant decrease
in symptoms is not noted, the dose should be increased every few weeks to a maximal dose of 25
to 30 mg weekly.
Injectable: 12.5-25mg per week
Effects: in 3-8weeks

98
Q

Methotrexate (DMARD) Contraindications

A

Methotrexate is contraindicated in pregnant and breastfeeding patients.
Contraindicated in those with leukopenia.
Those with immunodeficiency syndromes, renal impairment and liver disease. Methotrexate has many black box warnings: risk of
hepatotoxicity, renal impairment, pneumonitis, bone marrow suppression, diarrhea, ulcerative
stomatitis, dermatologic reactions, and opportunistic infections.

99
Q

Methotrexate (DMARD) Drug Interactions

A

Concurrent use with NSAIDs may increase the risk of bone marrow suppression and
gastrointestinal (GI) toxicity.

100
Q

RA vs OA Symptoms

A

RA Hallmark: Morning Stiffness that improves throughout the day
RA Hallmark: Symmetrical Arthralgias

101
Q

Difficult to Treat RA: D2T RA Definition

A

Presence or Absence of Inflammation
Mis-Dx or Co-existing disease

102
Q

D2T RA Guidelines

A

Shared decision making with treatment adherence.
Tailor DMARDs with Pt responses.
Co-mobidities impact QOL - consider!
Patients with concomitant HBV/HCV - DMARD management with hepatologist.
Non-Pharm: Diet, CBT, exercise!

103
Q

Hydroxychloroquine (Antimalarial) for RA Tx - MOA

A

Antimalarial inhibits antigen processing by elevating cellular pH, which changes antigen degeneration
Presentation of the antigen to T-Cells is impaired

104
Q

Hydroxychloroquine (Antimalarial) for RA: Dosing

A

200-400mg daily.
Therapeutic response seen 2-6mon after initiation.

105
Q

Hydroxychloroquine (Antimalarial) for RA: Contraindication

A

Pre-existing retinal filed changes.
Can decrease the metabolism of beta blockers.

106
Q

Fibromyalgia Diagnostic Criteria

A

Action-APS Pain Taxonomy (AAPT) Tool: 6 or more painful sites & sleep problems & Fatigue
9 total possible pain sites.

107
Q

Fibromyalgia Drug Treatment 1st Line

A

Pregabalin (Lyrica)
Duloxetine (Cymbalta)

108
Q

Pregabalin (Lyrica) for Fibromyalgia: MOA

A

Blocks some delta calcium channels, reducing neurotransmitter release. Antinociceptive effect.
AVOID: abrupt withdrawal

109
Q

Duloxetine (Cymbalta) for Fibromyalgia: MOA

A

Inhibits norepinephrine and serotonin reuptake.
Multiple indications: MDD, GAD, Neuropathic pain, MSK persistant pain

110
Q
A
111
Q

Gout Diagnostic Criteria

A

Synovial Fluid Analysis: Presence of monosodium urate monohydrate (MSU) crystals
Gram stain & culture: r/o septic arthritis

112
Q

Gout Genetic Testing & Race Considerations

A

Chinese, Thai, Korean, Native Hawaiian, or African American Ethnicities: test for the HLA B*5801 genetic variant.
Not eligible for Allopurinol due to severe cutaneous adverse risk if variant present!

113
Q

Colchicine in Gout Treatment MOA

A

Interferes with inflammasome complex assembly in neutrophils and monocytes, preventing IL1 activation (early is key!)
Concentrates PMN cells (subtype of leukocyte) and inhibits microtubule polymerization, preventing neutrophil migration and gout.
CYP450; 3A4 plus P-ap substrate sensitive

114
Q

Colchicine for Gout Treatment: Drug Interactions

A

Drugs that inhibit the CYP3A4 metabolic pathway
Ex: Atorvastatin, Bactrim, grapefruit juice, omeprazole, diltiazem, fluoxetine - Rhabdomyolysis risk!

115
Q

Colchicine for the Treatment of Gout: Dosing

A

Acute: 1.2mg PO x 1, 0.6 PO one hour later (Max 1.8mg dose/course)
Prophylactic: 0.6mg PO QD to BID (Max 1.6 QD)

116
Q

Colchicine for the Treatment of Gout: Caution

A

Renal or Liver patients
Fatal if given with P-ap or CYP3A4 Inhibitors!

Pharmacology for APRN (11 decks)

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