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Pharmacology > Lecture 2 (Rheum)-Exam 1 > Flashcards

Lecture 2 (Rheum)-Exam 1 Flashcards

1
Q

Extended-Release Products:
* Who is it reserved for?
* What does it decrease?
* Allow for what?
* What is there a high risk of?

A
  • Reserved for patients with severe chronic pain – usually cancer patients
  • Decreased dosing frequency
  • Allow for more even steady state with less peaks and troughs
  • High risk for overdose of accidently ingested or breach of extended-release mechanism (e.g., crushing, cutting, chewing)
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2
Q

What is a muscle spasm vs muscle spasiticity?

A

Muscle Spasm
* Sudden / involuntary
* Secondary to fatigue or injury

Muscle Spasticity
* Sustained contraction
* Decreased dexterity from the CNS
* Multiple sclerosis
* Cerebral palsy
* Stroke
* Spinal cord damage

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3
Q

What are approved muscle relaxants for muscle spasms?

A
  • Carisoprodol (Soma)
  • Chlorzoxazone (Parafon)
  • Cyclobenzaprine (Flexeril)
  • Metaxalone (Skelaxin)
  • Methocarbamol (Robaxin)
  • Orphenadrine (Norflex)
  • Tizanidine (Zanaflex)
  • Diazepam (Valium)
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4
Q

What are approved muscle relaxants for muscle spasticity?

A
  • Baclofen
  • Dantrolene
  • Tizanidine
  • Diazepam
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5
Q

How does a muscle contract happen?

A

Action potentials travel down the UMN from the central nervous system
* Cause release of excitatory neurotransmitters (glutamate, norepinephrine)
* Synapse with the LMN
* Activate muscle contraction

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6
Q

What is the inhibitory interneuron?

A

Regulates excitation of the LMN

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7
Q

Central inhibition of muscle contraction:
* How does Gaba work?

A

GABA – inhibitory neurotransmitter
* Binds to GABA receptors
* Causes cell hyperpolarization
* Decrease frequency of cell depolarization
* Decreasing muscle contraction

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8
Q

How does Benzodiazepines (diazepam, et al ) work?

A
  • Bind to GABA A receptors
  • Increases of Cl- influx
  • Hyperpolarization and decreased excitation

Work on CNS

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9
Q

How does baclofen work?

A

Binds to GABA B receptors
* Postsynaptic – increased K+ efflux
* Hyperpolarization

  • Presynaptic – decrease release of excitatory neurotransmitters (NE and glutamate)
    * Less action potentials

Work on CNS

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10
Q

How does Tizanidine work?

A
  • Alpha-2 agonist
  • Binds to alpha-2 receptors on presynaptic neurons of the UMN
  • Results in less release of exitatory neurotransmitters

Work on CNS

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11
Q

What are the four anti spasticity agents?

A

Baclofen, dantrolene, diazepam and tizinidine

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12
Q
A
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13
Q

What is the MOA of baclofen?

A

Binds GABAb receptors on:
1. LMN increasing K+ efflux, hyperpolarization, decreased action potential
2. Presynaptic UMN inhibiting release of excitatory NT glutamate and norepinephrine

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14
Q

What is the MOA of Dantolene?

A

Inhibits ryanodine receptors on the skeletal muscle cells; prevents Ca2+ release from SR preventing contraction

WORKS ON SKELETAL MUSCLE SO MORE PNS

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15
Q

What is the MOA of diazepam (Valium)?

A

Binds BDZ receptor on inhibitory GABAa receptor on LMN; increasing Cl- influx, hyperpolarization, decreased action potentials

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16
Q

What is the MOA Tizanidine (Zanaflex)?

A

Alpha-2 receptor agonist; binds to presynaptic UMN inhibiting release of excitatory NT glutamate and norepinephrine

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17
Q

What is unique about Dantrolene (Dantrium)?

A

Hepatotoxicity with high doses

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18
Q

What are the 6 antispasmodics medicine?

A
  • Carisoprodol (soma)
  • Chlorzoxazone (parafon)
  • Cyclobenzaprine (flexeril)
  • Metaxalone (Skelaxin)
  • Methocarbamol (Robaxin)
  • Orphenadrine (norflex)
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19
Q
A
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20
Q

What drug is a schedule IV that is antispasmodics?

A

Carisoprodol (soma)

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21
Q

What are the side effects of central muscle relaxants?

A
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22
Q

What are the Unique SE of central muscle relaxants?

A
  • Dizziness/ lightheadedness
  • Hypotension
  • Arrythmias
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23
Q

What are anticholinergic side effects?

A
  • Fever
  • Dry mucous membranes
  • Flushing
  • Blurred vision
  • mydriasis
  • Hallucinations
  • Sedation
  • Tachycardia
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24
Q

How are steroids produced?
* Released when?
* What type of effects?

A

Endogenous steroids produced in the adrenal gland (MC cortisol)
* Released in response to stress and inflammation
* Anti-inflammatory and immunosuppressive effects

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25
Q

What is the MOA of steroids?

A

Inhibit the production of inflammatory cytokines
* Bind to glucocorticoid receptors inside cells
* Bind to sites on DNA
* Down regulate cytokine production

Inhibit the production of inflammatory mediators
* Inhibit phospholipase A2
* Prevents the production of arachidonic acid
* Decreasing prostaglandins, leukotrienes, thromboxane

Immunosuppression

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26
Q

For steroids effects, what happens to the inflammatory response?

A

Suppress inflammatory response to all noxious stimuli
* Pathogens
* Chemical / physical
* Immune mediated / hypersensitivity

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27
Q

For the effects of steroids, how is inflammation reduced?

A

Reduce inflammation by DECREASING:
* Cytokine production – including various interleukins, tumor necrosis factor alpha
* Recruitment of WBCs and monocytes to sites of inflammation (neutrophil demargination)
* Lymphocyte, monocytes, basophil, eosinophil, mast cell production / function
* T-lymphocyte activity
* Production of prostaglandins, bradykinins, leukotrienes (inhibition of phospholipase A2)

Underlying cause of disease NOT corrected-> just a bandage

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28
Q

What is the short term adverse effect of steroids?

A
  • Increased appetite
  • Acne
  • Insomnia
  • Hyperglycemia – induction of gluconeogenesis and insulin resistance-> Caution with diabetes
  • Increased fluid retention, edema, and blood pressure
    * Mineralocorticoid effects
  • Mood / Psychiatric changes
  • Steroid psychosis
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29
Q

What is the long term adverse effect of steroids?

A
  • Hypothalamic – pituitary-adrenal axis suppression
    * Cushing syndrome – moon facies, buffalo hump, central obesity
  • Growth suppression (in younger people)
  • Muscle wasting
  • Skin atrophy
  • Immunosuppression (issues with infection)
  • Cataracts / glaucoma
  • Decreased bone mineral density (need to watch closer)
  • Gastrointestinal bleeding
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30
Q

What are the big effects of glucocorticoids and mineralocorticoids?

A

Glucocorticoids
* Glucose metabolism
* Anti-inflammatory

Mineralocorticoids
* Sodium retention
* Fluid retention

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31
Q
A
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32
Q

What drug is high glucocorticoid and no mineralocorticoids?

A

Dexamethasone

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33
Q

Tapering

What is the recommedation following prolonged use/higher doses of steroids?

A

Recommended following prolonged use / higher doses
* Prednisone ≥ 30 mg daily (or equivalent) for ≥ 2 weeks
* Any dose systemic steroid for ≥ 4 weeks
* Signs and symptoms of HPA suppression present

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34
Q

Why do you need to taper steriods?

A

Used to avoid disease flare or adrenal crisis/insufficiency (HPA suppression)

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35
Q

LOW YIELD

What is the general taper for steroids?

A
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36
Q

What is the signs and symptoms of adrenal insufficiency?

A
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37
Q

Osteoporosis:
* What is the mechanism?
* What is less?
* Who is at higher risk of fracture?
* What is thinning?

A
  • Osteoclasts break down bone faster than osteoblasts rebuild it
  • Fewer trabeculae
  • Bones with higher percentage of trabecular bone at increased risk of fracture – spine, wrist, ribs
  • Cortical bone thinning
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38
Q

What is the most common casues of osteoporosis?

A
  • Postmenopausal dt decreased estrogen
  • Age related
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39
Q

How does postmenopausal cause osteoporosis?

A

Postmenopausal - decreased estrogen
* Increased proliferation, differentiation, and activation of osteoclasts (more breakdown)
* Increased calcium excretion (increase Ca in pee)
* Decreased calcium absorption from the GI tract

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40
Q

How is age related issues cause osteoporosis?

A
  • Osteoblasts lose ability to form bone
  • Osteoclasts retain activity
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41
Q

What are the risk factors of osteoporosis?

A
  • Decreased estrogen
  • Decreased serum calcium
  • Alcohol consumption
  • Smoking
  • Medications (steroids, heparin)
  • Physical inactivity
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42
Q

What is the t-scores and diagnostic criteria for osteoporosis?

A
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43
Q

Who needs to be screened for osteoporosis?

A
  • All adults ≥ 50 years with history of fracture
  • USPSTF: all women ≥ 65 years
  • Endocrine society: all men ≥ 70 years
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44
Q

What is a bone healthy lifestyle?

A
  • Weight-bearing exercises with resistance training – 30 to 40 min, three times a week
  • No Smoking
  • Limited ETOH
  • Fall prevention
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45
Q

How much calcium should women take pre and postmenopausal?

A
  • 1000 mg daily – premenopausal women and men 50 to 70 years of age
  • 1200 mg daily – postmenopausal women and men 71 years and older
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46
Q

How much vitamin D should women and men take? What does it do?

A
  • 600 international units/ day men and women 51 to 70 years
  • 800 international units / day – men and women > 70
    * Reduce bone loss and fracture rate in older men and women taking adequate calcium
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47
Q

How much protein do you need to intake for osteoporosis prevention?

A

0.8 g/kg/day

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48
Q

What are the high risk patients of osteoporosis?

A
  1. Patients with osteopenia and a history of fragility fracture at the hip or spine
  2. Patients with a t-score of -2.5 or less in the lumbar spine, femoral neck, total hip
  3. Patients with a T-score between -1 and -2.5 if the FRAX 10-year probability of major osteoporotic fracture ≥ 20% and hip fracture ≥ 3%
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49
Q

What is the first line therapy of osteoporosis? How does it work?

A

Bisphosphonates

MOA:
* Reduce bone resorption by:
* Stimulating osteoclast apoptosis
* Decrease cholesterol synthetic pathway which decreases osteoclast function

Osteoclasts are either killed or unfunctional

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50
Q

What is the pharmacokinetics of bisphosphonates?

A

Bioavailability poor - < 1%
* Worse with concomitant food intake

Amount absorbed
* 50% eliminated renally
* 50% remains for months to years

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51
Q

What are the side effects of bisphosphonate?

A
  • Esophagitis
  • Esophageal irritation
  • Heartburn
  • Abdominal pain
  • Diarrhea
  • Hypocalcemia
  • Renal dysfunction
  • Osteonecrosis of the jaw – rare, prolonged, high doses, invasive dental procedures ⭐️
  • Flu-like symptoms (fever, muscle aches) with IV therapy
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52
Q

Bisphosphonates:
* What are the oral medicine?
* What should you do to increase bioavailability and decrease SE?

A

Oral (alendronate, risedronate, ibandronate)
* Take on empty stomach in the morning – increases poor bioavailability
* Full glass of water
* Remain upright for at least 30 minutes

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53
Q

What are the IV bisphosphonates?

A

Intravenous
* Zoledronic acid
* Pamidronate

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54
Q

What are drug holidays for bisphosphonates?

A
  • After 3 to 5 years treatment – patients mild to moderate fracture risk
  • After 6 to 10 years – patients at high fracture risk
  • ≤ 5 year holiday with BMD Q 2 to 4 years

You can stop taking the medicine

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55
Q

What are the second line treatments of osteoporosis?

A
  • Denosumab
  • Ralonifene
  • Teriparatide

Patients who cannot tolerate or have contraindications bisphosphonates

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56
Q

How are specific agents determined for osteoporosis?

A

Specific agent depends on patient co-morbidities, T-scores, adverse effects, patient preference

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57
Q

What is densumab used for?

A

Patients at high risk for fracture (eg, osteoporosis by BMD in the absence of fragility fracture, T-score >-2.5 with a fragility fracture, single vertebral fracture)

Osteoporosis

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58
Q

What is raloxifene used for?

A

Patients with no history of fragility fractures, especially in women at high risk for breast cancer

osteoporosis

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59
Q

What is teriparatide used for

A

Patients at very high risk of fracture (eg, T-score of ≤-3.5, T-score of ≤-2.5 plus a fragility fracture, severe or multiple vertebral fractures)

osteoporosis

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60
Q

What is the mechanism of action and CI for denosumab, teriparatide and raloxifene?

A
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61
Q

What are the adverse effects and specific features of denosumab, teriparatide and raloxifene?

62
Q

Osteoporosis
* What do you need to obtain after therapy?
* When does less frequent monitoring for osteoporosis occur?

A
  • Obtain a follow-up dual-energy x-ray absorptiometry (DXA) of the hip and spine after two years
  • Less frequent monitoring if BMD better or stable
63
Q

What do you need to evaluate the patient for if they have clinically significant BMD decrease or a new fracture after therapy?

A

Evaluate patient for:
* Poor adherence
* Inadequate gastrointestinal absorption
* Inadequate intake of calcium and vitamin D
* Development of a disease or disorder with adverse skeletal effects.

64
Q

What do you need to do with patients who have a decrease in BMD (<5 percent) no discernible contributing factors after osteoporosis treatment?

A
  • Continue the same therapy and repeat BMD two years later OR
  • Switch therapies
65
Q

What is the treatment goals of osteoarthritis?

A
  • Minimize pain
  • Optimize function
  • Slow the process of joint damage
66
Q

What is the the mainstay of OA management and should be tried first?

A

Nonpharm interventions:
* Weight management and exercises
* Physical therapy for knee OA; not effective for hip OA
* Braces and foot orthoses not recommended
* Glucosamine / chondroitin not recommended

67
Q

What is the first line therapies for OA?

A
  • Acetaminophen
  • Topical NSAIDS
  • Systemic NSAIDS
  • Capsaicin
68
Q

why is acetaminophen given as a first line for OA?

A

Acetaminophen less effective than NSAIDs but initial trial
appropriate given superior safety profile

69
Q

Why is topical NSAIDs use as a first line for OA after acetaminophen?

A

Topical NSAIDS (e.g., diclofenac) moderately effective
* Trial recommended for minimal joint involvement (knee)
* Recommended over systemic NSAIDs for patients ≥ 75 years of age

70
Q

Why are systemic NSAIDs given as a first line drug for OA after acetaminophen and topical NSAIDs?

A
  • Systemic NSAIDs effective; give at lowest effective dose to minimize side effects; as needed dosing appropriate
  • Patients < 75 years
  • Patients at low risk for gastrointestinal or cardiovascular events
71
Q

What drug is used for hand osteoartrisitis only?

72
Q
  • What are the drugs are second line of OA? Explain why you use them
A

Tramadol
* Patients not responding to acetaminophen, NSAIDs (alone or in combination)
* Patients with high GI or CV risk
* Minimal role for other opioids

Duloxetine
* Moderate efficacy for knee OA
* Add on therapy for patients with low to moderate response to first-line therapies

73
Q

What can be used as first line for OA if local ?

A

Intra-articular corticosteroid injections
* Patients not responding to acetaminophen, NSAIDs (alone or in combination)
* Improve function and provide short-term pain control; no improvement in QOL
* Triamcinolone or methylprednisolone
* Frequency – every 3 months
* Risk of greater cartilage loss

74
Q

What is last line for OA?

A

Surgery
* Last line therapy
* Improve function and provide pain relief for patients with moderate to severe pain and radiographically confirmed OA

75
Q

For RA, what is the disease process?

76
Q

What are the different types of DMARDs? (synthetic and biologic)

77
Q

What is the first line for RA? And how does it work?

A

Methotrexate

  • Inhibits tetrahydrofolate reductase; inhibits DNA synthesis / cell proliferation
  • Primarily rapidly dividing inflammatory cells
78
Q

methothrexate

What are the contraindications, SE and what do you need to mointor?

79
Q

What is the moa, contraindication, SE and monitoring needed for Lefluomide?

A

For RA-synthetic DMARDs

80
Q

What is the DOC for pregnancy for RA-synthetics?
* What are the SE and what do you need to monitor?

81
Q

What is the sulfasalazine’s MOA, contraindication, SE and monitoring?

A

RA-Synthetic DMARDs

82
Q

LY

Jannus Associated Kinase (JAK) inhibitors – tyrosine kinase inhibitors
* How does it work?
* What is an example?
* What are the side effects?

83
Q

What are antibodies and what are monoclonal antibodies?

A

Monoclonal antibodies: antibobies made in the lab that target certain receptors

84
Q

What are the sites of action for Rituzimab, Tocilixumab, abatacept, and anakinra?

85
Q

RA-biologic DMARDs:
* What is there is increase risk of?
* What do you need to screen for?
* What do you need to give before therapy?
* What do you not give during therapy?

A

Increased risk of infection – reactivation of TB / varicella zoster
* Screen patient for TB, hepatitis B and C, HIV, and vaccine status prior to initiation
* Give appropriate vaccination before therapy initiation
* Give influenza and pneumococcal vaccines as needed during therapy
* Do not give live vaccines during therapy

86
Q

RA-biologic DMARS:
* What do you need to monitor for?
* Regimen may require holding depending on what?
* What is a common reaction?

A
  • Monitor patient closely for signs / symptoms of infection
  • Regimen may require holding depending on severity of infection
  • Infusion reactions common – patients may require premedication and rescue medication
    * Hydrocortisone - diphenhydramine - epinephrine
87
Q

What is the same across the board for biologic DMARDs for RA?

A

ALL are subcutanous or IV

88
Q

How do you figure out the severity of RA?

A

Severity
* Multiple methods to determine
* Disease Activity Scale (DAS – 28)
* Number of swollen joints
* ESR or CRP level
* Global Patient Health Score (0 to 100)

  • < 2.6 = remission
  • 2.6 to 3.2 = low
  • > 3.2 = moderate to severe
89
Q

What are the treatment goals of RA?

A

Treat to target
* Remission
* Low disease activity

90
Q

How do you give inital symptomatic relief as a bridging therapy for RA?

A

NSAIDS and / or steroids
* Rapid onset of action
* Control inflammation and decrease pain
* NSAIDS do not modify disease process
* Steroids considered disease modifying antirheumatic drugs (DMARDs) but risk of long-term use outweigh benefits

Symptom relief but does not control disease progression

91
Q

How do you control the disease progression of RA?

A

DMARDS
* Inhibiting immune response and blocking proliferation endothelial cells and fibroblasts at involved joint
* Specific mechanisms vary
* Slow onset of action – weeks to months
* Stop or slow the disease process – remission is possible

NSAIDs+steroids with DMARDs then tapper off steroids

92
Q

What is the first line of RA?

A

Methotrexate
* Oral administration conditionally preferred over subcutaneous injection

93
Q

For RA treatment:
* What is not recommended?
* Why is methotrexate recommended?
* What is there strong evidene of?
* What is methotrexate similar to?

A
  • HCQ and SSZ not recommended – limited disease modifying effects
  • Easy dosing/inexpensive since once a week
  • Strong evidence supporting use in combination therapy
  • Similar efficacy to biologic DMARDS with better safety profile and lower financial burden
94
Q

When should you do monotherapy and combination therapy for RA?

A
  • Monotherapy appropriate if low disease activity
  • Combination DMARD therapy if moderate to high disease activity
95
Q

What is also added for initial therapy for moderate to high RA?

A

Glucocorticoids
* Short-term therapy recommended in addition to DMARD therapy for patients who require for symptom resolution
* Therapy initiation
* Disease flairs
* Toxicity > benefit for long-term use in all patients
* Long-term therapy NOT recommended
* Lowest dose for shortest time

96
Q

What is the second line monotherapy for RA? What is the dual therapy?

A

Second-line monotherapy - biologic or tofacitinib
* No specific biologic recommended

Dual therapy (add bio to methotrexate)
* May be required for patient with moderate to high disease activity
* MTX + biologic DMARD
* MTX + tofacitinib

97
Q

RA:
* What is triple therapy?
* All therapies have what?
* Choice of drug depends on what?
* When switching therapies for lack of efficacy, what do you do?

A

Triple therapy = MTX/HQ/SSZ

All therapies with similar long-term outcomes
* Choice dependent on resource setting and patient comorbidities
* When switching therapies for lack of efficacy; switching to biologic DMARD of different class recommended

98
Q

What is the treatment for Juvenile idiopathic arthritis (JIA)- Oligoarthritis?

99
Q

What is the treatment for juvenile idiopathic arthritis (JIA)-Polyarthritis?

100
Q

What are the non-pharmacotherapy and first line therapy for acute gout flare?

A

Non-pharmacotherapy:
* Ice / rest

First-line pharmacotherapy:
* NSAIDs – any NSAID is appropriate; including COX-2 specific agents
* Systemic corticosteroids – prednisone most common but could use alternatives
* DOC if NSAID contraindications
* Colchicine

101
Q

What are the second line therapy for acute gout flare?

A

Intra-articular corticosteroids – monoarticular disease, rule out septic arthritis

102
Q
  • What is the treatment (dosages)?
  • When should you consider switching drugs?
103
Q

Colchicine:
* What is the MOA?
* When most effective?

A
  • Anti-inflammatory – disrupts microtubule formation preventing activation, degranulation, and migration of neutrophils
  • Most effective when started within 36 hours of symptom onset
104
Q

What is the contraindications of colchicine?

A

P-glycoprotein or strong CYP3A4 inhibitors – mostly protease inhibitor used for the treatment of HIV (e.g., ritonavir)

105
Q

What are the adverse reactions of colchicine?

A
  • Diarrhea
  • Nausea / vomiting
  • Pharyngolaryngeal pain
  • Bone marrow suppression (leukopenia, granulocytopenia, thrombocytopenia, aplastic anemia)

GI SE!!!!!!

106
Q

What are the lifestyle modifications for chronic treatment of gout?

107
Q

When is urate lowering therapy recommended or not recommended for chronic gout?

A

Urate lowering therapy (ULT) strongly recommended for patients with:
* ≥ 1 subcutaneous tophi
* Radiologic evidence of damage attributed to gout
* ≥ 2 acute gout flares/year

Urate lowering therapy (ULT) conditionally recommended for patients with:
* Greater than one but less than two acute gout flares/year

Urate lowering therapy (ULT) NOT recommended for patients after first flare except for under specific circumstances – see guidelines

108
Q

What is the first line therapy and alternative therapies for chronic treatment?

A

First line therapy: Allopurinol
* All patients – including those with stage ≥ stage 3 CKD

Alternative therapies
* Febuxostat
* Probenecid
* Colchicine

109
Q

GOUT – CHRONIC TREATMENT (ULT)

  • When should chronic gout treatment be started?
  • What is concomitant initial therapy with?
  • What is target uric acid levels?
A

All therapies should be started after resolution of acute gout flare
* Concomitant initial therapy with anti-inflammatory prophylaxis for 3 to 6 months is strongly recommended (low dose colchicine or NSAIDs)-> because increase risk of acute flare
* Doses should be increased to a target serum uric acid level of <6mg/dL

110
Q

Hyporicemics:
* What are the exampes and what is the MOA?
* What are the SE?

A

Allopurinol and febuxostat:
* Decrease formation of uric acid by inhibiting xanthine oxidase

Allopurinol side effects:
* Rash
* Acute gout flare
* Nausea/vomiting
* Hepatic failure/hepatic necrosis

111
Q

Uricosurics:
* What are the examples?
* What is the MOA?
* Increase risk of what?

A

Probenecid and sulphinpyrazone
* Decreased uric acid reabsorption from the kidneys by competing for uric acid transporter
* Increased risk of kidney stone formation

112
Q

Pseudogout:
* What are the non-pharmcotherapy txt?
* What is the pharmcotherapy for acute flare? Chronic ?

113
Q

What are the treatment goals of reactive arthritis?

A
  • Identify triggering infection STD
  • Treat ACTIVE infection (ex. STI)
  • Prompt treatment of organism can prevent initiation and persistence of arthritis
  • Less evidence for treating of post-enteric infections (GI bug)
114
Q

Reactive arthritis?

When treating of organism can prevent initiation and persistence of arthritis, what is the treatment for PRC positive chlamydial infections?

A

Best data PCR positive Chlamydial infections
* Prolonged treatment (3 to 6 months) recommended
* Doxycycline + rifampin OR azithromycin + rifampin
* Symptom remission and PCR negativity

115
Q

What is first line, second line txt of reactive arthritis?

A

First-line NSAIDs
* Two to 4-week trial on full dose prior to changing NSAIDs

Second-line glucocorticoids - patients who do not respond to NSAIDs
* Intra-articular preferred for mono or oligoarthritis
* Systemic treatment indicated for patients with polyarthritis
* Three to 6-month trial before moving to next step

116
Q

What are the symptoms for reactive arthritis?

117
Q

What is the treatment for chronic forms for reactive arthritis?

A
  • Conventional systemic DMARDs – methotrexate / azathioprine
  • Biologic DMARDs – etanercept / infliximab

Reactive into chronic

118
Q

What are the treatment goals of fibromyalgia?

A
  • Confirm diagnosis
  • Patient education KEY
  • Evaluate and treat / control the major symptoms § Chronic widespread pain
    * Fatigue
    * Insomnia
    * Cognitive dysfunction
  • Goal = improve quality of life
119
Q
  • What are the symptoms of fibromyalgia?
  • How should treatment be dealt with?
A

Treatment should be individualized, multidisciplinary, and involving both nonpharmacologic and pharmacologic therapy in most patients

120
Q

What are the non-pharm treatments for FM?

A
  • Acupuncture
  • Biofeedback
  • Cognitive behavioral therapy
  • Exercise
  • Hypnotherapy
  • Massage
  • Meditation
  • Guided imagery
121
Q

Fill in the pharmacotherapy for FM

122
Q

What is polymyositis and dermatomyositis?

123
Q

What is inital therapy for polymyositis?

124
Q

What are additional therapies and what do you need monitor for polymyositis?

125
Q

What is polymyalgia rheumatica?

126
Q

What is the initial therapy of POLYMYALGIA RHEUMATICA?

127
Q

What are additional therapies and what needs to be monitor for POLYMYALGIA RHEUMATICA?

128
Q

What is POLYARTERITIS NODOSA (PAN)?

129
Q

What is the initial therapy of PAN (servere and non-severe)

A

Methylpresidone

130
Q

What are adiitional therapies and monitoring needed for PAN?

131
Q

What is the treatment for Sjogren’s

A
  • Mainly symptomatic with goal of keeping mucosal surfaces moist
  • Artificial tears or saliva, increased hydration, ocular and vaginal lubricants
  • Pilocarpine improves symptoms by stimulating the exocrine glands
  • Cyclosporine may improve ocular symptoms
  • Hydroxychloroquine-may help arthralgias
  • Glucocorticoids-not effective for sicca symptoms but may have role in treatment of extraglandular manifestations
132
Q

SJOGREN’S DISEASE – SICCA SYMPTOMS

133
Q

Cyclosporine (restasis):
* What does it cause?
* What type of drug is it?
* How much time do you need to wait inbetween eye drops?

A
  • Increase tear production in keratoconjunctivitis sicca-associated ocular inflammation
  • Immunomodulator / anti-inflammatory
    * Inhibition of T-cell activation
  • Allow ≥15mins between dosing of lubricant eye drops.
134
Q

What are the adverse reactions of cyclosporine (restasis)

A
  • Ocular burning
  • conjunctival hyperemia
  • Eye pain
  • Foreign body sensation
  • Pruritus, stinging, blurring
135
Q

PILOCARPINE (SALAGEN):
* What does it cause?
* What are contraindications?
* What are precautions?

A

Cholinergic agonist; increases secretion of exocrine glands

Contraindications:
* Uncontrolled asthma
* Miosis undesirable (iritis, acute angle- closure glaucoma)

Precautions:
* Severe hepatic impairment

136
Q

PILOCARPINE (SALAGEN):
* What are the interactions?
* What are adverse reactions?

A

Interactions:
* Cardiac conduction disturbances with β- blockers.
* Antagonizes anticholinergics (eg, atropine, ipratropium)

Adverse Reactions:
* Sweating
* Nausea
* Rhinitis
* Flushing
* Urinary frequency
* Abnormal vision

137
Q

Scleroderma symptoms?

138
Q

Scleroderma:
* Is there a cure?
* How is treatment individualized?
* What is the goal?
* Multiple specialist involvement due to what?
* Treatmet is aimed at what?

139
Q

SCLERODERMA – RAYNAUD’S:
* What do you need to educate your patient on?
* What is first line therapy?

A

Reduce frequency and severity of attacks

Patient education:
* Smoking cessation
* Cold avoidance
* Avoid vasoconstricting medications

First-line therapy:
* Calcium channel blockers (dihydropyridine-type)
* Ex: Nifedipine or amlodipine

140
Q

What is the MOA for calcium channel blockers?

A
  • Bind to and blocks voltage-gated calcium channels
  • Calcium does not enter the cell
  • No depolarization
  • Muscle does not contract
  • Vasodilation
141
Q

What are the symptoms of lupus?

142
Q

What is the goals of lupus?

A
  • Improve long-term survival
  • Prevent organ damage
  • Prevent disease flares
  • Optimize quality of life
  • Complete remission rare
    Most patients can obtain partial remission / low disease activity in all or most organs
143
Q

LY

What is mild, moderate, severe lupus?

A

Based on systemic lupus erythematosus disease activity index

144
Q

What is the adjunct, treatment of non renal systemic lupus erythematosus? What are the goals?

145
Q

What is first line of SLE?

A

First-line (Grade A):
* Hydroxychloroquine (DMARD)
* Glucocorticoids (e.g., prednisone)
* Rapid symptom control
* Short-term therapy recommended or daily dose of ≤ 7.5 mg/day

146
Q

What is second line of SLE?

A

Methotrexate or azathioprine
* Methotrexate more effective
* Azathioprine compatible with pregnancy

Cyclosporine (CNI)
Mycophenolate mofetil

147
Q

What is the txt for patients with SLE and extra renal disease? What is the MOA?

A

Belimumab (Grade A moderate refractory)
* MOA: B-lymphocyte stimulator antagonist
* Recommended for:
* Patients with inadequate control of extra renal disease
* Ongoing disease activity or frequent flare

148
Q

Belimumab is more likely to respond in patients with what?

A
  • SLEDAI score > 10
  • Prednisone dose > 7.5mg/day
  • High complement levels
149
Q

What are drugs that are high and low risk of drug induced lupus?

150
Q

Drug induced lupus:
* What are the clinical features?
* When does it start?
* All patients ahve what?
* Improvement when?

A
  • Clinical features predominantly constitutional, joint, & pleuropericardial
    * Rare CNS & renal disease
  • Months to years after starting offending agent
  • ALL patients have antinuclear antibodies (ANA)
  • Improvement following withdrawal of offending drug

Pharmacology (14 decks)

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