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Pharmacology II > Exam 1 - Rheumatology Meds > Flashcards

Exam 1 - Rheumatology Meds Flashcards

1
Q

Inflammatory Response of RA

A
  • Immune system = overactive
  • Symmetrical manifestations. Extra-articular manifestations as well.
  • Cell membrane is damaged; releases arachodonic acid
  • AA is converted to LOX and COX
  • LOX => leukotrienes
  • COX => prostaglandins
  • Leads to neutrophils formed; damage tissue and cause free radical species.
  • B cells produce plasma cells, which form antibodies
  • Antibodies and complement system attacks PMNs
  • PMNs release cytotoxins and free radicals promoting cellular damage
  • T cells recruit chemokines - TNF-alpha and IL
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2
Q

Pannus

A

Chronic inflammation of the synovial tissue; pannus invades cartilage and bone surface leading to erosion and destruction of the joint.

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3
Q

What drugs prevent histamine, kinins, and prostaglandins from being produced?

A
  • NSAIDs

- Corticosteroids (first line for acute RA flare ups)

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4
Q

OA has apoptosis of chrondrocytes. What supplements will regenerate chondrocytes?

A

Glucosamine

Chondroitin

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5
Q

Pharmacologic Therapy for RA:

A

Chronic treatment

  • NSAIDs
  • Low dose corticosteroids

Acute exacerbations
-Corticosteroids

DMARDS
-Disease modifying anti-rheumatic drugs

Knee effusions

  • Aspiration of fluid
  • Corticosteroid injection
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6
Q

Pharmacologic Therapy for OA:

A

Chronic Treatment

  • Acetaminophen!
  • NSAIDs
  • Topical analgesics for local pain (Capsaicin)

Acute exacerbations
-Opioid analgesics

Knee effusions

  • Aspiration
  • Corticosteroid injection; don’t use systemic corticosteroids for OA
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7
Q

Why do we want to initiate DMARDS as soon as possible in RA?

A

They can slow disease progression down.

NSAIDs and corticosteroids are only for symptomatic relief.

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8
Q

What are the traditional or non-biologic DMARDs?

A

Methotrexate (Rheumatrex)
Hydroxychloroquine (Plaquenil)
Sulfasalazine (Azulfidine)
Leflunomide (Arava)

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9
Q

What drug is an abortificant?

A

Methotrexate

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10
Q

What are the Biologic DMARDs that bind to TNF to inactivate it and arrest the inflammatory cascade?

A

Monoclonal antibodies (-mab):

  • Infliximab (Remicade)
  • Certolizumab (Cimzia)
  • Etanercept (Enbrel)
  • Adalimumab (Humira)
  • Golimumab (Simponi)

MOA: Biologics bind to TNF to inactivate it and arrest the inflammatory cascade.

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11
Q

What Biologic DMARD is a co-stimulation modulator?

A

Abatacept (Orencia)

MOA: Co-stimulation modulator:

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12
Q

What Biologic DMARDs are CD20 receptor antagonist?

A

Tocilizumab (Actemra)
Rituximab (Rituxan)

MOA: CD20 receptor antagonist

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13
Q

What Mixed DMARD is a JAK inhibitor?

A

Tofacitinib (Xeljanz)

  • Newest drug for RA
  • Works as a tyrosine kinase inhibitor

-Between a biologic and non-biologic

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14
Q

What other agents are used to treat RA, albeit, less often:

A 
Azathioprine (Imuran)
D-penicillamine
Gold
Anakinra (IL-1 receptor antagonist)
Cyclosporine (Neoral)

Gold or heavy metals are poisonous to cells. Immune system rapidly produces new cells. Give gold to inhibit inflammatory cascade.

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15
Q

What are the most frequently used Non-biologic DMARDs?

A

Methotrexate and hydroxychloroquine:

  • Best efficacy/toxicity ratios.
  • Methotrexate and corticosteroids are continued for a long time - Good combination to delay progression of disease.
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16
Q

Why is MTX used first?

A

MTX - should be started first on most patients with RA.

  • Most evidence behind use.
  • Good component for multi-drug regimens if you need to add on another drug.
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17
Q

How long do traditional or non-biologic DMARDs take for action?

A

Slow onset of action

  • 3-6months until full effect.
  • Faster affects with MTX, sulfasalazine, and leflunomide in 1-2 months.

Give patient 3-6 months before you decide therapy won’t work.

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18
Q

How long do biologic DMARDs take for action?

A

May provide benefit within a couple of weeks.

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19
Q

Whats a concern with using DMARDs for therapy?

A
  • Lead to immunosupression.
  • Can lead to increased risk of infection.
  • TB testing done prior to therapy.
  • Vaccinations should be up to date.
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20
Q

Why is TB testing done before putting a patient on Biologic DMARD therapy?

A

Don’t want to have latent TB and have it be activated by these drugs.

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21
Q

Vaccine recommendations for those on biologic DMARDs:

A
  • Give vaccinations before Biologic DMARD is given

- When you can generate good antibodies against particular infection.

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22
Q

What vaccinations can be given during therapy with DMARDs?

A

Killed, recombinant, and inactivated vaccines can be given during therapy

  • Pneumococcal
  • IM flu shot
  • Hepatitis B

Do NOT give LIVE vaccines for patients on biologics or immunosuppressed.

ACR: Recommends herpes zoster at 50yo.

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23
Q

When is it appropriate for a patient to be given a live attenuated virus vaccine?

A

Give it to them before starting DMARD therapy or not at all.

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24
Q

Methotrexate MOA

Trexall, Rheumatrex

A

MOA: Blocks synthesis of purines, which generate DNA in new cells.

  • Analog of folic acid
  • Binds to DHF reductase stronger than folic acid will
  • Prevents cells from using folic acid; can’t make purines
  • Leads to cell death

Toxicity from non-biologic DMARDs is rapidly reproducing cells. - GI tract, alopecia, immune system takes a hit bc they constantly producing new WBCs.

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25
Q

Methotrexate Toxicity

A
  • Bone marrow suppression
  • GI/oral ulceration or stomatitis (oral mucosa can’t replicate as quickly).
  • Hepatotoxicity - metabolized by liver, excreted by kidneys
  • Alopecia

Less alopecia than you’d see in a cancer patient, because its a smaller dose.

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26
Q

Why is it important for patients to drink a lot of water when on MTX?

A

Stay well hydrated; if you become acidotic, it will precipitate in kidneys and cause AKI.

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27
Q

Contraindications of MTX

A
  • Pregnancy (abortificant)
  • Poor renal function, CrCl < 40ml/min (increase risk of AKI)
  • Chronic liver disease can become worse.
  • Blood dyscrasias - thrombocytopenia, leukopenia - will worsen bone marrow suppression.
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28
Q

MTX pros

A
  • Most commonly used DMARD
  • Effective, fairly rapid onset of action (1-2 months)
  • PO, SubQ, IM
  • Monitor: CBC, LFT, SCr

Give folic acid 1mg/day to help limit chronic side effects of MTX.

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29
Q

What do you give in MTX overdose?

A
  • Folic acid is not converted to active form.

- Give Folinic acid (Leukovorin), used for MTX rescues.

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30
Q

Leflunomide (Arava)

A
  • MOA: inhibits pyrimidine synthesis
  • Decreased lymphocyte proliferation
  • Decreases RA symptoms, inflammation, and joint damage (comparable to MTX)
  • Benefits seen in a month

-Monitor: LFT, CBC, pregnancy

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31
Q

Leflunomide (Arava) ADR

A

-Diarrhea, hepatotoxicity, and hematologic toxicity.

Teratogenic

  • Undergoes enterohepatic recirculation
  • Takes months to eliminate; problematic for pregnancy
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32
Q

What is given to patients on Leflunomide to reduce levels more quickly?

A

Cholestyramine

  • Bile Acid Sequestrant
  • Eliminates levels more quickly by pulling med from GI tract before its reabsorbed in the biliary tract.

“Cholestyramine clean out”

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33
Q

Hydroxychloroquine use

A
  • Good for mild RA disease
  • Less toxic, least potent non-biologic DMARD
  • Response in 2-4mos.
  • LESS monitoring; not assoc. w/ myelosupression, hepatotoxicity, or renal sufficiency = GOOD
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34
Q

Hydroxychloroquine MOA

A
  • Inhibits neutrophil locomotion
  • Decrease chemotaxis eosinophils
  • Impairs complement-dependent antigen-antibody reactions
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35
Q

Hydroxychloroquine ADR

A
  • N/V/D - take with food
  • Retinopathy - monitor visual acuity at start of therapy and after.
  • Increased skin pigmentation.
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36
Q

Sulfasalazine

A

Prodrug: Cleaved by colonic bacteria, converted into sulfapyridine and 5-aminosalicylic acid.

  • Modulates inflammatory mediators and inhibits actions of TNF.
  • Mechanism unknown.
  • Response 1-4 months; use 6 months for full efficacy
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37
Q

Why do you “start low and go slow” with sulfasalazine?

A
  • N/V/D
  • Rash
  • Elevated LFTs
  • Alopecia
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38
Q

Sulfasalazine - Drug RXNs

A
  • Bound up by FQs, macrolides, iron supplements.
  • Might have increased bleeding effect with warfarin.
  • Kicks albumin off of cells, makes warfarin work more effectively.
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39
Q

Sulfasalazine SE

A

Tell patient it turns urine and stools yellow and orange.

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40
Q

What is the “go to” non-biologic DMARD?

A

MTX

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41
Q

What’s a good non-biologic to use for mild disease?

A

Hydroxychloroquinone

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42
Q

Tofacitinib (Xeljanz) MOA

A
  • Works to inhibit JAK protein.
  • IL and TNF bind to JAK receptors, work to modulate transcription of inflammatory mediators (STAT proteins).

By inhibiting JAK tyrosine kinase, STAT proteins are not activated
-Inhibiting STAT proteins decreases inflammatory gene transcription

  • Available orally
  • Test for latent TB before admin.
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43
Q

How are mabs administered?

A

IV only

Nonbiologics = oral admin.
Biologics (mabs) = IV admin.

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44
Q

Tofacitinib (Xeljanz), a Mixed DMARD, is used by itself or in combination with other DMARDS.

  • Multiple non-biologics is ok
  • Mixing non-biologic and biologic is ok
  • Mixing Tofacitinib (Xeljanz) with non-biologic or biologic - its ok

NEVER combine two biologics together. Why?

A

Too much immunosupression, risk for secondary infections, and death.

On the test, two biologics, the answer you would NOT give to your patient.

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45
Q

What is BLACK BOX warning for Tofacitinib (Xeljanz)?

A

Serious infections, increased risk for lymphoma and other malignancies.

Levels of this drug can be increased by CYP3A4 inhibitors or renal impairment.

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46
Q

Why do you have to be careful when prescribing Tofacitinib (Xeljanz) with a patient on a CYP3A4 inhibitor?

A

Levels of this drug can be increased by CYP3A4 inhibitors.

Also can see an increase in renally impaired pts.

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47
Q

Biologic DMARDs

Naming note:
U - human protein
XI - mouse/human protein

A
  • Effective in treating RA, esp. if they failed MTX and other non-biologic DMARD treatment!
  • VERY expensive.
  • Very little monitoring, less risk of systemic toxicity
  • Less risk of hepatic injury and alopecia

Effective immunosupression:

  • Increased risk for infection, viral/bacterial, and TB.
  • ALWAYS test for TB before giving biologic drug.
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48
Q

If a patient on a biologic DMARD has an infection, what do you do?

A

Discontinue drug, so they have an immune system to fight.

Do NOT give LIVE vaccines.

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49
Q

Contraindications

TNF-a inhibitors

A
  • Worsen CHF
  • Increased CV death with infliximab and etanercept
  • Bad for late stage HF patients or if they have a poor ejection fraction
  • Worsen MS by inducing symptoms
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50
Q

Blackbox warning: TNF-a inhibitors?

A

Lymphoproliferative cancer

-Do risk/benefit analysis

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51
Q

Etanercept (Enbrel)

A

BIOLOGIC DMARD

  • MOA: Binds to and inhibits TNF, which decreases inflammation and slows damage.
  • Two TNF receptors link to the FC fragment of IgG. You have two TNF receptors, so they bind to TNF and inactive them.
  • Can use in combination with MTX (non-biologic).
  • SubQ 2x/wk, given parenterally (pens or infusion).
  • Risk of ANAPHYLAXIS, injection site reactions.
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52
Q

Infliximab (Remicade)

A
  • XI: Chimeric antibody - mouse and human IgG (allergic risk).
  • Second line therapy to MTX.

MOA: Binds to and inhibits TNF resulting in less inflammation and joint damage.

Risk: Body can produce antibodies to drug, causing drug can be less effective. Some patients need to receive MTX with it, so body won’t release antibodies to the drug. MTX will suppress immune system to keep the drug efficacious.

Won’t prevent anaphylaxis; just allows you to have this drug working longer.

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53
Q

Administration of Infliximab (Remicade)

A

3mg/kg IV followed by 3mg/kg IV 2 and 6 weeks after first dose, then repeateated every 8 weeks there after.

Infused over 2 hrs.

High risk of injection reactions; have anaphylaxis kit available - epinephrine, diphenhydramine, corticosteroids.

Start at a slow rate, see how they do, and gently titrate up for 2 hours.

Allergic RXN, but effective tx: Need to desensitize them by infusing over 8hrs.

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54
Q

Adalimumab (Humira) MOA

A
  • U: Human monoclonal antibody specific for TNF-alpha

- Binds to TNF-a and renders it inert to decrease inflammatory symptoms / joint damage

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55
Q

What’s a benefit to the make up of Adalimumab (Humira)?

A
  • Its an all human antibody

- Lower allergy risk than infliximab (Remicade).

56
Q

When is it appropriate to use Adalimumab (Humira)?

How is it administered?

A
  • Indicated for patients who have had inadequate response to MTX.
  • Second line therapy.
  • Can be used as a monotherapy (by itself) for RA.
  • Self-administered pen (every other week)
  • Easier admin than Infliximab, which is infused (every 6-8wks).
57
Q

Adalimumab (Humira) ADR

A
  • Increased risk for infections.
  • Latent TB infections could be activated.
  • Injection site reactions
  • Rash, HA, pruritus.
58
Q

Abatacept (Orencia)

A

BIOLOGIC DMARD

  • Third line agent for those who failed TNF-alpha inhibitor.
  • Co-stimulation modulator, used in moderate to severe disease.
  • MOA: Binds to CD80/CD86 receptors on immune cells to prevent interaction between APCs and T cells.
  • Prevents T cell activation and stops inflammation of joints.

-Administered every 4 weeks. -Biologics have a long half-life, bc they’re proteins and aren’t degraded as quickly as MTX.

59
Q

Rituximab (Rituxan)

A
  • XI: human and mouse antibody
  • Third line therapy: Once pt failed MTX and TNF-a blockers
  • MOA: Targets CD20 protein on B-lymphocytes, binding to it causes a complete depletion of B cells and decreases antigen presentation to T cells.
  • When drug is D/C’d, it takes a while for B cell levels to recover.
60
Q

Why do you have to give a pre-treatment to patients taking Rituximab (Rituxan)?

A

Rituxan has a lot of injection site reactions.

Pre-treatment:
Need to administer 1st. gen. antihistamines and steroids
-Diphenhydramine
-Methylprednisolone.

Have anaphylaxis kit available with epinephrine to prepare for a severe allergic reaction.

61
Q

Tocilizumab (Actemra)

A
  • MOA: Targets IL-6 in the inflammation cascade
  • Used after failure of TNF blockers
  • Hepatic damage, elevated transaminases
  • GI perforation

INDUCES CYP3A4

62
Q

When putting a patient on Tocilizumab (Actemra), what drug interactions should you plan for?

A

Tocilizumab (Actemra) induces CYP3A4.

Induction of CYP3A4 metabolism will reduce levels of other drugs: 
-Warfarin
-Birth Control
-Statins
Those drugs will be less effective.
63
Q

Failure of Biologic DMARDs

A

-30% failure rate

  • Primary lack of efficacy - failure to see response 3-6 months after starting
  • Secondary lack of efficacy - failure after initial good response to maintain response

-Some pts will quit therapy because of adverse effects.

64
Q

What do you do if you initiate biologic DMARD treatment on a pt and the therapy isn’t working?

A

Add a non-biologic for synergistic therapy:

  • Hydroxycloroquine
  • Methotrexate
  • Leflunomide
65
Q

If you start a patient on a TNF inhibitor that isn’t working, what can you switch them to?

A

Switch to another biologic DMARD that’s “stronger”

  • Rituximab - targets B cells
  • Actemra - targets IL6

Switch MOA if first biologic doesn’t work effectively.

66
Q

Why would you change from one TNF inhibitor to another?

A

Infliximab requires you to go to an infusion center every two months, where Humira can be given to yourself every two weeks with injections.

Can switch to make it more convenient for patient based on their preference.

67
Q

Corticosteroids MOA

A

MOA:
-Work on steroid receptors in nucleus to change gene transcription factors to prevent inflammatory mediators from being made.

  • Interfere with antigen presentation to T cells
  • Inhibit PG and LT production
  • Inhibit free radical generation
  • Impair chemotaxis
68
Q

If a patient is on corticosteroids for more than one week, why is it important to taper the dose?

A

Adrenal insufficiency

69
Q

How do we use corticosteroids in Chronic RA?

A

Chronic: Patients require low dose oral corticosteroids everyday. .

  • Not favorable due to side effects
  • Every other day administration is ineffective.
70
Q

Why do we use corticosteroids as a “bridge therapy”?

A

Bridge therapy: Patients switching from one type of DMARD to another, so CS can be used as a bridge to help maintain remission until DMARDs start kicking in.

71
Q

What type of corticosteroids do we use for acute flare ups?

A

Disease flare up - get back to baseline. PO.

  • IM - short acting for burst therapy - methylprednisolone
  • Long acting depot forms - natural taper and have less withdrawal.
72
Q

When do we use intra-articular injections of corticosteroids?

A

Intra-articular injections - less systemic reactions, good for those who have less joints affected.

73
Q

Why can’t you do intra-articular injections of corticosteroids more than 2-3x per year?

A

Can’t administer for more than 2-3x per year

Can have increased joint destruction from impaired healing and tendon atrophy.

74
Q

Corticosteroids dosing….

A

Use the lowest dose possible to limit systemic side effects.

Will slow progression of disease for first few years.

75
Q

Corticosteroids ADR

A 
HPA axis supression 
Adrenal insufficiency
Osteoporosis
Myopathies
Cataracts
Hirsutism
Hyperglycemia
Hyperlipidemia
Infection risk
76
Q

OA Treatment

A

Tylenol and acetaminophen are used for control, but NSAIDs can be added.

77
Q

RA Treatment

A

NSAIDs are used with corticosteroids; don’t help with disease progression. Used to manage symptoms only.

78
Q

COX-2 inhibitors

A
  • Better for patients at high risk of GI issues.

- Avoid in patients with CV history.

79
Q

What NSAID is given to a patient with: low risk for GI complications?

A

Non-selective NSAID

80
Q

What NSAID is given to a patient with: high risk for GI complications?

A

Use NSAID, plus a gastroprotective agent like misoprostol or PPI.

COX-2 inhibitor can be used if they have low CV risk.

81
Q

What NSAID is given to a patient with: high risk for CV disease?

A

Use non-selective NSAID if necessary.

82
Q

Low to high disease severity tx?

A

MTX +/- prednisone

83
Q

Moderate to high disease severity tx?

A

MTX +/- hydroxychloroquine
Infliximab +/- MTX
TNF inhibitor

84
Q

Moderate to high disease activity with TNF inhibitor failure?

A

Non-TNF biologic
Rituximab +/- MTX

If monotherapy with TNF inhibitor, add MTX

85
Q

If therapy with TNF inhibitor and MTX does not work, what do you switch to?

A

Keep MTX

Tofacitinib +/- MTX

86
Q

If a patient has a moderate to severe disease, but had a non-TNF biologic failure, what do you put them on?

A

Add a different TNF biologic with MTX.

Still not working… Move to Tofacitinib +/- MTX.

87
Q

What combination therapies are used in non-biologic DMARDs?

A

MTX + hydroxychloroquinone
MTX + sulfasalazine
MTX + hydroxychloroquinone + sulfasalazine

MTX + leflonomide = high risk of hepatotoxicity

88
Q

Why is it bad to prescribe MTX with Leflunomide?

A

High risk of hepatotoxicity; skip this combination.

89
Q

What combination therapies are used in non-biologic DMARDs when combined with biologic DMARDs?

A 
MTX + etanercept
MTX + infliximab
MTX + adalimumab
Leflunomide + Infliximab
MTX + anakinra
90
Q

NEW ONES

Acetaminophen

A
  • First line for analgesia in OA
  • Mild to moderate disease
  • Less effective than NSAIDs, but has less toxicity
  • Scheduled therapy for pain coverage

Risks:

  • Hepatotoxicity - make sure they don’t consume over 4 grams.
  • Warfarin - Acetaminophen makes warfarin more effective

Monitor AST, ALT, PT/INR

91
Q

Topical Analgesics

  • Diclofenac (Voltaren gel)
  • Salicylate prodts. (Aspercreme)
A

Topical NSAIDs

  • Multi-joint OA
  • First line for knee pain with OA when acetaminophen is CI/failed.
  • Preferred over oral NSAIDs, bc less systemic side effects.
92
Q

Capsaicin

A
  • Topical analgesic
  • Has to be used consistently to deplete substance P
  • Used with other analgesics for synergism.

Counter-irritants

  • Menthol, camphor, oil of wintergreen
  • Create cold/heat over sore surface to help to counteract that pain
93
Q

Intra-articular Corticosteroids

A

Alternative first line therapy for knee and hip OA when not controlled on NSAIDs or acetaminophen.

Don’t administer more than 3x per year - tendon atrophy and joint destruction can occur.

94
Q

Opioids and OA

A

Second line therapy; to be used short-term

95
Q

Glucosamine and Chondroitin

A
  • Safe, natural products found in cartilage and synovial fluid
  • MOA: Increase proteoglycan synthesis and help to repair cartilage
  • Moderate improvement in symptoms May have disease modifying effects.
  • Dietary supplements (not as well regulated by FDA).

-AVOID if you have a shellfish allergy

96
Q

Hyaluronate Injections

A

Intra-articular injections; most often used for OA of knee

  • Constituent of synovial fluid
  • Has anti-inflammatory properties; reduces pain and improves mobility
  • Given once a week for 3-5weeks
  • No side effects
97
Q

If OA pt can’t tolerate acetaminophen (first line for OA), what do you use?

A

Topical NSAIDs

IN ORDER

  • Followed by intra-articular corticosteroids
  • Tramadol
  • Oral NSAIDs good if younger pts and no CV/GI risk.
98
Q

How much acetaminophen can you give to a patient with OA who has cirrhosis/alcoholism?

A

3g/day

  • Chronic alcoholics
  • Cirrhosis
99
Q

If first-line OA therapies failed, what do you give pt?

A

Opioid analgesics
Surgery
Diloxetine (NE reuptake inhibitor)
Intra-articular hyaluronic acid.

100
Q

How do you treat a 75 year old patient with hand OA?

First line therapy

A

Older than 75:

  • Topical NSAIDs - better to help spare the kidneys and liver.
  • Topical Capsaicin
  • Tramadol

Younger patients:

  • Oral NSAIDs
  • Topical capsaicin
  • Tramadol

If not working:

  • Combine therapy with NSAIDs and capsaicin
  • NSAIDs and tramadol
101
Q

What medications are associated with osteoporosis?

A

Aromatase inhibitors - decrease estrogen

Furosemide - increase calcium excretion

Proton pump inhibitors - decrease calcium absorption

102
Q

What hormones affect bones?

A

Estrogen
Testosterone
PTH - important to regulate calcium levels via osteoclast activity

103
Q

What is the active form of vitamin D used to stimulate calcium absorption and retention?

A

1,25 dihydroxy vitamin D (Calcitrol)

  • Needs to be given in an active form
  • Otherwise, liver would need to activate it
104
Q

What increases osteoclast activity?

A

Lack of estrogen.

Stimulation of PTH will stimulate bone breakdown to increase blood levels of calcium.

105
Q

Non-pharmacologic therapy for osteoporosis and osteopenia: Calcium

A
  • Supplied as calcium carbonate
  • ADR: constipation, hypercalcemia, nephrolithiasis
  • Binds to a lot of drugs in GI tract, need to space out - take meds 1 hour before or 4 hours after
  • iron, thyroid supplements, FQs, tetracyclines, bisphosphates
106
Q

Non-pharmacologic therapy for osteoporosis and osteopenia: Vitamin D

A

Vitamin D

  • Patients with hepatic or renal dysfunction CANNOT recieve ergo/cholecalciferol (D2/D3).
  • Taken in through diet

Calcifediol made in liver
Calcitriol made in kidney

107
Q

If a patient has poor renal function and hepatic function, what form of vitamin D can they have?

A

Calcitriol

Otherwise they won’t have an active form of Vitamin D

108
Q

If a patient has poor hepatic function, what form of vitamin D can they have?

A

Calcifediol

Kidneys can activate it to calcitriol.

109
Q

What are standards for a patient to recieve pharmacologic therapy?

A
  • Osteoporosis
  • Low bone mass
  • 10yr probability of osteoporosis related fracture
110
Q

Bisphosphonates

  • Alendronate (Fosamax)
  • Ibandronate (Boniva)
  • Risedronate (Actonel)
  • Zoledronic acid (Reclast)
  • -IV ONLY ONE
A

-MOA: Agents mimic pyrophosphate, which is an endogenous bone resorption inhibitor that reduces osteoclast maturation and lifespan.

  • Poor bioavailability <1%
  • Food/drink will decrease it
  • Absorbed and incorporated into bone, XS is renally eliminated
  • Half life is 10 years
  • IV option: 100% bioavailability
111
Q

Bisphosphonates ADR

A

ADR: heartburn, dyspepsia, can’t take with food – may see esophageal erosion or ulcer.
Can see osteonecrosis of the jaw.

112
Q

How are Bisphosphonates administered??

A

Take tablets with 6oz of water; NO other liquids or drug will not be absorbed.

  • Take 30mins before other foods/liquids
  • Sit upright for 30mins so drug will get past esophagus
  • IV form can be useful if they can’t swallow.
113
Q

Denosumab (Prolia)

A

MOA: Monoclonal antibody, which prevents RANK-L from binding to RANK receptor so cells won’t mature into osteoclasts.

RANK-L, which binds to RANK receptor of osteoclast precursor cells to promote maturation.

  • Given SubQ.
  • Peak concentration in 10 days
  • Half life 25 days
  • Dosed every 6 months
114
Q

Denosumab (Prolia) ADR

A

ADR: local reactions, skin infection, bone turnover supression

115
Q

Mixed Estrogen Agonist/Antagonists

Raloxifene (Evista)

A

Raloxifene (Evista)
-Estrogen agonist and antagonist

-Benefit: have antagonist effects in breast tissue to prevent cancer but agonist effects in the bone

116
Q

Calcitonin

A
  • Not recommended for osteoporosis unless other therapies failed
  • Endogenous hormone released from the thyroid gland when calcium is elevated
  • Reduces calcium levels

Intranasal administration
Reduces vertebral fractures (not hip)

Used for hypercalcemia.

117
Q

Teriparatide (Forteo)

A

Used on patients with high risk for fractures that failed bosphosphonate therapy.

-MOA: Anabolic agent to stimulate bone formation, decrease remodeling, and stimulate osteoblast activity

Take drug less than 2 years!!!!!! OTHERWISE AT RISK FOR BONE CANCER

118
Q

For patients with low risk for fractures, normal bone density - What therapy do you put them on?

A
  • Dietary calcium and vitamin D supplements
  • Smoking cessation
  • Limit OH intake
119
Q

For patients with low bone mass and higher risk of fracture?

A

Medications to reduce loss of bone:

  • Alendronate
  • Zoledronic acid
  • Denosumab

If you’re failing therapy:

  • Raloxifene
  • Intranasal calcitonin
120
Q

Acute Gouty Arthritis Tx:

A

NSAIDs, corticosteroids, colchicine

Start ASAP, combination therapy for those in severe pain with multiple joints being affected

121
Q

Triamcinolone acetonide

A
  • Corticosteroid; can be oral or intra-articular route.
  • Used for RA, OA
  • Long duration of action, not systemic
  • If >2 jts affected, systemic therapy needed
  • If they’re on corticosteroids for over one week, taper dose to avoid renal insufficiency
122
Q

Colchicine (Colcrys)

A
  • Anti-mitotic; important to pull apart DNA during reproduction. Prevents cell replication.
  • MOA: Binds to microtubules in neurtophils to limit inflammtory response where crystals are deposited in gout.

-Used for acute gout attacks witin 36hrs.

ADR:

  • GI effects N/V/D
  • Can lead to NEUTROPENIA and neuromyopathy
123
Q

Mild to moderate pain, gout tx?

A

NSAID
Colchicine
Systemic corticosteroid

124
Q

Severe pain, gout tx?

A

Combination
Colchicine + NSAID
Colchicine + corticosteroid

125
Q

For patients who are more prone to recurrent gout attacks, what would help them?

A
  • Decrease purine intake, meats, etc.
  • Eliminate uric acid using urate therapy
  • Can be put on colchicine as a prophylactic.
126
Q

What medications can raise uric acid levels?

A

Thiazide and loop diuretics
Niacin
Low dose aspirin

127
Q

Urate Lowering Therapy

A
  • Cost effective for those with two or more attacks per yr.

- Considered when one or more tophus is present

128
Q

What drugs decrease synthesis of uric acid?

A

Xanthine oxidase inhibitors

Xanthine oxidase inhibitors stop conversion of hypoxanthine to xanthine to uric acid. (more hypoxanthine, less uric acid).

Decreases chance of another attack.

129
Q

What drugs increase uric acid excretion?

A

Uricosurics

130
Q

Xanthine Oxidase Inhibitors

  • Allopurinol (Zyloprim) ADR?
  • Febuxostat (Uloric)
A

MOA: Xanthine oxidase inhibitors stop conversion of hypoxanthine to xanthine to uric acid. (more hypoxanthine, less uric acid).

  • Well tolerated
  • Allopurinol (Zyloprim): rash, more rare - TENS, exfoliative dermatitis
  • If pt can’t tolerate allopurinol, put them on Febuxostat (Uloric
131
Q

Uricosuric drugs

-Probenecid

A
  • MOA: increase renal clearance of uric acid by inhibiting post-secretory renal tubule reabsorption.
  • High levels of the uric acid will then be in renal tubules could lead to nephrolithiasis!

XO inhibitors more frequently used. Don’t have this risk.

132
Q

Probenecid ADR

A

ADR:

  • Precipitation of acute gout
  • May increase levels of drugs - PCN, cephalosprins by inhibiting renal excretion.
133
Q

Rasburicase (Elitek)

A
  • Used for cancer patients
  • Recombinant form of urate oxidase, breaks uric acid down to allatantoin (soluble form) for excretion.
  • In Leukemia, those cells are broken: tumor lysis syndrome
  • See kidney dsyfunction secondary to that for cancer pts.
  • Can also give them allopurinol to stop uric acid from forming in the first place.
134
Q

Rasburicase (Elitek) ADR

A

Patients can develop autoantibodies that decrease efficacy of this drug.

  • Allergy
  • Hemolysis and hemoglobinemia in patients with GG6PD deficiency!!
135
Q

How do we manage patients that have no indication for urate lowering therapy?

A

Should be on diet modifications and avoid diuretics and niacin.

136
Q

How do we manage a patient that needs urate lowering therapy and has recurrent episodes of gout throughout the yaer?

A

First line:

  • Allopurinol - 1st
  • Febuxostat

Alternative:
-Probenecid

Gout prophylaxis:

  • Colchicine
  • Low dose NSAIDs

Pharmacology II (10 decks)

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