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PHARM 557 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

XO (xanthine oxidase) inhibitors

A

Allopurinol, febuxostat, oxipurinol

-XO converts metabolites into uric acid

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2
Q

4 clinical phases of gout

A
  1. Asymptomatic hyperuricemia
  2. Acute gouty arthritis (gout attack)
  3. Intercritical gout
  4. Chronic tophaceous gout
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3
Q

Hyperuricemia

A

Serum uric acid over 420umol/L

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4
Q

Gout is more likely caused by…

A

Under-excretion of uric acid

Rather that overproduction of uric acid

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5
Q

Podagra

A

Big toe is affected in gout commonly

  • then works its way up
  • due to lower body temp and decreased urate solubility
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6
Q

Tophi

A

Urate deposits - a later complication of hyperuricemia - uncommon

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7
Q

Common comorbidities the precipitate gout

A

HTN

Renal dysfunction

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8
Q

3 options for tx of gout

A

NSAIDs
Colchicine
CSs
-all first line

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9
Q

Any NSAID can be used in gout as long as…

A

It’s max dose

  • Naproxen 500mg BID
  • Ibuprofen 800 QID
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10
Q

Length of NSAID therapy in gout

A

Take for 10 days and then stop - taper not often needed

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11
Q

Colchicine doing for gout

A
  1. 2mg now, then 0.6mg in 1hr

- can continue with 0.6mg OD-BID until resolved, or for prophylaxis

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12
Q

Common oral prednisone dose for gout

A

25-50mg x 3-5days

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13
Q

Prophylactic tx in gout?

A

Frequent attacks - more than 2-3 a year

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14
Q

The issue with NSAIDs, colchicine, and CSs in gout

A

Does NOT correct hyperuricemia or prevent tophi

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15
Q

Goal for gout in terms of serum urate level

A

Less than 400umol/L

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16
Q

Allopurinol dosing for goal

A

Initial dose of 100mg daily

Maintenance dose of 300mg daily

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17
Q

Take how long for allopurinol to work in gout

A

6 months

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18
Q

Osteoarthritis definition

A

Chronic, progressive disorder characterized by the loss of articulate cartilage in primarily hands, knees, spine, and hips

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19
Q

Osteoarthritis is a …… disorder of the joint

A

Degenerative

-has biochemical and inflammatory sx

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20
Q

Pathogenesis of osteoarthritis

A

Imbalance between cartilage maintenance and destruction

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21
Q

Clinical feature of osteoarthritis

A

Joint pain with activity

  • happens later in the day
  • RA is right when you wake up

Pain improves with rest, stiffness doesnt last more than 30mins

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22
Q

Osteoarthritis inflammatory disease?

A

No

RA is

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23
Q

Diagnosis of osteoarthritis

A

No reliable test to dx so hx is very important

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24
Q

4 pillars of treatment for osteoarthritis

A
  1. Pt education
  2. Rehabilitation
  3. Meds
  4. Referrals - dietician, PT/OT, surgery
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25
Q

Osteoarthritis - exercise

A

Avoiding high impact things

-biking and swimming are GOOD

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26
Q

Most effective and under-utilized interventions for osteoarthritis

A

Non-pharm interventions

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27
Q

Oral DOC for osteoarthritis

A

Acetaminophen

  • use high doses to be effective
  • up to 1g QID
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28
Q

NSAID that has least CV risk

A

Naproxen

-and low dose celecoxib

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29
Q

Antidepressant used in osteoarthritis

A

Duloxetine

-not dosed prn

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30
Q

Hyaluronic Acid injection for what site of osteoarthritis

A

Knee

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31
Q

CSs injections for osteoarthritis

A

Used for acute inflammation

-lasts 4-8weeks, not to be used more than q3months

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32
Q

4 main concerns with NSAIDs/COV2 inhibitors

A

GI bleeds
CV risk
Renal function
DIs

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33
Q

Advantage of COX2 inhibitor over NSAIDs

A

Less GI toxicity risk

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34
Q

Etiology of SLE

A

Genetically predisposed and then triggered by something else

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35
Q

Clinical features of SLE

A

Fatigue
Fever
Weight loss

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36
Q

To be dx with lupus need at least 4 of the following:

A
  • malar rash
  • discoid rash
  • renal disorder
  • photosensitive
  • oral ulcer
  • arthritis
  • neurologic disorder
  • hematologic disorder
  • immunologic disorder
  • serositis
  • anti-nuclear antibodies
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37
Q

Tx of SLE depends on

A

Severity and location of disease

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38
Q

Drug-induced Lupus drugs

A

Procainamide
Hydralazine
Quinidine
Methyldopa

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39
Q

Ankylosing Spondylitis affects 2 parts of the body

A

Spine

Sacroiliac joint

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40
Q

Ankylosing spondylitis definition

A

A chronic systemic inflammatory rheumatic disorder

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41
Q

Ankylosing spondylitis- spinal mobility

A

80% lose spinal mobility within 10yrs of onset

  • usual time to dx is 9yrs
  • vertebrae in lumbar spine start fusing together
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42
Q

First line therapy for ankylosing spondylitis

A

NSAIDs

-decrease x-ray progression!

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43
Q

Second line therapy in ankylosing spondylitis

A

TNF blockers

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44
Q

Status epilepticus

A

Usually anything over 5 mins - can last up to 1 hr

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45
Q

Epilepsy dx

A

Greater than or equal to unprovoked seizures separated by a 24hr period
-no underlying problem that can be corrected (tumor, infection, alcohol withdrawal)

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46
Q

Peak incidence for epilepsy

A

Teen and seniors

-approx 60% of NEW pts are young children and elderly

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47
Q

Drug therapy for epilepsy dictated by….

A

Based on SE profile

  • not a lot of efficacy differences
  • some make certain subtypes worse though
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48
Q

Pathophysiology of seizures

A

Too much excitation - glutamate
Too little inhibition - GABA
-or a mixture of both

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49
Q

Clinical Manifestations of seizure depend on 3 things

A
  1. Site of focus
  2. Degree of irritability of the surrounding brain area
  3. Intensity of the impulse
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50
Q

4 main types of seizures

A
  1. Partial (folal)
  2. Generalized
  3. Unclassified
  4. Status epilepticus
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51
Q

2 subtypes of partial seizures

A

Simple and Complex

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52
Q

5 subtypes of generalized seizures

A
  1. Absence
  2. Tonic-clonic
  3. Myoclonic
  4. Atonic
  5. Infantile Spasms
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53
Q

Only subtype of generalized seizures that may have an aura

A

Tonic-clonic

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54
Q

Tonic-clonic seizures

A

Stiff tone convulsions

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55
Q

Myoclonic seizures

A

Brief, bilateral shock-like contractions - jerks

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56
Q

Atonic seizures

A

“Drop Attack”

-LOC, sudden loss of muscle tone

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57
Q

Brian imagine in epilepsy

A
  • not to observe seizure activity

- ID structural abnormalities (lesions)

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58
Q

Achievable goals in epilepsy

A
  • decrease in number of seizures
  • prevent seizure recurrence
  • prevent/minimize AEs of AEDs
  • optimizable QOL (employment, driving)
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59
Q

Why is monotherapy preferred in epilepsy?

A
  • fewer AEs
  • increases probability of adherence
  • more cost-effective
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60
Q

MOA of the type of AEDs

A
  • enhance GABA
  • inhibit glutamate
  • neurotransmitter focused
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61
Q

Titration process for AEDs

A
  • start at 1/4-1/3 of the initial target dose (except phenytoin, could give therapeutic dose right away)
  • gradully increase q1wk over 3-4wks to target dose (except lamotrogine, should be q2wk due to rash AE)
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62
Q

How to switch out monotherapy for AEDs

A

Gradually withdraw first agent after maintenance of second agent is achieved, and well-controlled
-would try 2-3 agent as monotherapy before combining therapies

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63
Q

Factor favouring successful d/c of AEDs

A

Seizure free - 2yrs for absences, 4yrs with any other type
Hx of single type of seizure
Hx of low frequency of seizures
Normal neuro exam
Children - can stop after 6 months seizure free

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64
Q

Stopping AED treatment

A

No optimal rate of withdrawal for AED, but a schedule of at least 6 wks seems safe

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65
Q

Type A AEs for AEDs

A
  • related to the known MOA of drug, so expected

- drowsiness, fatigue, cognitive impairment

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66
Q

Type B AEs for AEDs

A
  • related to individual vulnerability (immunological, genetics)
  • rashes, hepatotoxic effects
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67
Q

Type C AEs for AEDs

A
  • relate to the cumulative dose of the drug
  • MOSTLY reversible
  • weight gain/loss, decreases BMD, hirsutism
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68
Q

Type D AES for AEDs

A
  • related to prenatal exposure to the drug (teratogenesis) or carcinogenesis
  • irreversible
  • birth defects, neurodevelopmental delay
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69
Q

Type E AEs for AEDs

A
  • adverse drug interactions

- increased skin rash reaction, reduced seizure control, reduced effectiveness of warfarin

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70
Q

First line drugs for generalized tonic-clonic seizures

A
  • carbamazepine
  • lamotrogine
  • oxycarbazepine
  • valproate
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71
Q

First line drugs for focal seizures (both simple and complex)

A
  • carbamazepine
  • lamotrogine
  • oxycarbazepine
  • levetiracetam
  • valproate
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72
Q

First line drugs for absence (petit mal) seizures

A
  • ethosuximide - only used in absence and kids
  • lamotrogine
  • topiramate
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73
Q

First line drugs for myoclonic seizures

A
  • topiramate
  • levetiracetam
  • valproate
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74
Q

First line drugs for atonic or clonic seizures

A

-valproate

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75
Q

MOA of carbamazepine

A

Ion channel mediator

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76
Q

Advantages of carbamazepine

A
  • minimal cognitive impairment
  • minimal weight gain
  • option for aggressive pts
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77
Q

Disadvantages of carbamazepine

A
  • self-induced metabolism
  • decreases effectiveness of OCP
  • teratogenic
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78
Q

MOA of Gabapentin - epilepsy

A

Ion channel modifier

-may have a link to GABA

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79
Q

Advantages of gabapentin

A
  • No know PK DIs
  • does NOT decrease effectiveness of OCP
  • well tolerated
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80
Q

Disadvantages of gabapentin

A
  • may worsen Myoclonic seizures
  • teratogenic
  • heavy pill burden
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81
Q

Place in therapy for ethosuximide

A

1st line for absence seizures, limited to kids

-should not be used in any other seizure type (even if mixed type included absence)

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82
Q

MOA of lamotrogine

A

-inhibits Na channels and inhibits glutamate

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83
Q

Advantages of lamotrogine

A
  • weight neutral
  • considered most safe AED in pregnancy
  • used for bipolar disorder as well
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84
Q

Disadvantages of lamotrogine

A
  • DI with valproate - use lower dose of lamotrogine
  • very slow titration (q2wks)
  • OCP reduced lamotrogine levels
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85
Q

Main AE of lamotrogine

A

RASH

-reason for slower titration up

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86
Q

MOA of levetiracetam

A

Inhibits GABA action

87
Q

Place in therapy of levetiracetam

A

Pts have likely failed other agents before going on this one

88
Q

Main AE with levetiracetam

A

Somnolence

And psych SEs

89
Q

MOA of Phenytoin

A

Ion mediator

90
Q

Place in therapy for phenytoin

A

Not used as first line

  • generalized tonic-clonic and complex partial
  • during or following neurosurgery
91
Q

Disadvantages of phenytoin

A

Inducer of CYP P450 so MANY DIs

-decreases folate, vit D, and vit K levels

92
Q

MOA of valproate

A

GABA-ergic drug

93
Q

Place of therapy for valproate

A

Can be used in almost all seizure types

94
Q

MOA of diazepam

A

Enhances GABA effects

95
Q

Place in therapy for diazepam

A

Short-term management

-including status Epilepticus

96
Q

Place in therapy of lacosamide (vimpat)

A

Adjunctive therapy for partial seizures in adults

-not used by itself

97
Q

Disadvantages of valproate

A

Most risk in pregnancy

98
Q

All women on AEDs should take …..

A

5mg folic acid per day prior to any pregnancy

99
Q

Diet for epilepsy

A

Ketogenic diet
90% fat, 7% protien, 3% fat

Great benefit in kids!

100
Q

Surgery is an option in epilepsy only for….

A

Focal epilepsy

101
Q

Recommendations to improve public safety on APAP

A

Lowering max daily dose

Lowering max unit dose

Dosing devices

Labelling/packaging

102
Q

APAP primarily metabolized in the ….

A

Liver

103
Q

NAPQI toxicity causes

A

Hepatotoxicy by hepatocyte death

104
Q

Phase 1 of APAP toxicity

A

0-24hr

-NV, diaphoresis, anorexia

105
Q

Phase 2 of APAP Toxicity

A

18-72hrs

  • reduction of phase 1 sx, could be asymptomatic
  • increase in liver enzymes
  • RUQ pain
106
Q

Phase 3 of APAP toxicity

A

72-96hr

  • “do or die” phase
  • will either survive this, or succumb to liver failure
  • jaundice, hepatic Encephalopathy, fulminant hepatic failure
  • death
107
Q

Phase 4 of APAP toxicity

A

4days-3wks

  • if pt makes it to this phase, will go into recovery
  • complete resolution of sx
  • liver will return to how it was before insult
108
Q

Key info to gather in APAP Toxicity

A

Time of ingestion

109
Q

Most important diagnostic tool in APAP toxicity

A

Plasma APAP level

-directly tells us how to treat using nomogram

110
Q

Limits of APAP nomogram

A
  • at-risk populations
  • pts presenting later than 24hrs
  • chronic/repeated Supratherapeutic ingestions
  • MR products
111
Q

Toxic dose of APAP

A

Single dose: greater than 7.5g or 150mg/kg (peds as well)

112
Q

First thing to do when pt presents with APAP toxicity

A

Supportive care and ABCs!

113
Q

When to used SDAC in APAP Toxicity

A

If within 4 hrs possibly

114
Q

APAP suitable for hemodialysis?

A

Yes

-low PPB, low Vd, and under 500 daltons

115
Q

Antidote for APAP toxicity

A

NAC

-n-acetylcysteine

116
Q

MOA for NAC

A

Maintains glutathione levels

117
Q

At what hour does benefit of NAC go down

A

8hrs

-when glutathione levels are less than 30%

118
Q

NAC IV Dosing - 150mg/kg = …. ml

A

200ml D5W or NS

119
Q

NAC IV Dosing - 50mg/kg = … ml

A

500ml D5W or NS

120
Q

NAC IV Dosing - 100mg/kg = … ml

A

1000ml D5W or NS

121
Q

NAC oral option?

A
  • longer regimen (72hr)
  • highly emetogenic
  • better outcomes in late presenting pt (over 12hrs)
122
Q

When do you draw APAP serum levels

A

4hrs post-ingestion

-draws all other lab tests immediately (INR, glucoes, enzymes)

123
Q

When would you give NAC always immediately

A
  • after 8hrs

- would still draw samples, but give antidote while waiting to get back levels

124
Q

When cant you use APAP nomogram

A

Repeated Supratherapeutic Toxicity (staggered OD)

125
Q

NAC for staggered OD

A

Start if ALT>50 IU/L or APAP conc >132umol/L

  • check levels again after 8hrs
  • continue if ALT >50 IU/L or APAP conc >66umol/L
126
Q

Pathophysiology of RA

A

Autoimmune response

  • chronic inflammation of synovial tissues results in growth of this tissue
  • this inflamed, growing synovial tissue is called pannus
127
Q

Clinical Presentation of RA

A

Joint pain and stiffness for more than 6 weeks

  • needs to last more than 6 weeks to have dx
  • tenderness and swelling
128
Q

Lab tests for RA

A

ESR and CRP increased - if these are normal, likely not RA
Rheumatoid Factors - iffy
Anemia
Synovial fluid turbid due to leukocytes

129
Q

Less commonly affected joints in RA

A

Hips and neck

-RA usually affects joints symmetrically on both sides

130
Q

Urgency in dx of RA?

A

Yes

-joint damage is irreversible

131
Q

Extra-articulate involvement in RA

A 
Rheumatoid nodules - non-tender
Vasulitis 
Pulmonary compilations (fibrosis, pneumonitis)
Ocular
Cardiac
132
Q

Diagnosis of RA scored based on 4 categories:

A
  1. Joint involvement (number and size)
    - the more joints effected, the more likely it is RA
  2. Serology (RF and/or ACPA)
  3. Acute phases reactants (CRP and/or ESR)
  4. Duration of sx - has to be over 6 weeks
133
Q

Goal of RA management

A

Always remission of the disease!

134
Q

Definition of improvement for RA

A

ACR20

  • greater than 20% improvement in tender joint count, swollen joint count
  • pain rating, ESR or CRP, global assessment
135
Q

4 treatment option for RA

A

DMARDs
Biologics
CSs
NSAIDs

136
Q

How long do DMARDs take to work in RA

A

No immediate effect

1-3 months to work

137
Q

DMARDs used in RA

A 
Hydroxychloroquine (Plaquenil)
Sulfasalazine 
MTX
Leflunomide
--> others: gold, cyclosporine, azathioprine, minocycline
138
Q

Usual dose of MTX for RA

A

7.5-25mg po qwk

139
Q

What should always be given with MTX in RA?

A

Folic acid

1-5mg per day suggested to decrease SEs

140
Q

Hydroxychloroquine useful in RA?

A

Yes and very safe

-only good for mild case though

141
Q

Backbone/standard therapy for RA

A

MTX

-mod-severe RA

142
Q

Biologics in RA on the market

A 
All TNF antagonists: cytokine blockers
Entanercept (Enbrel)
Infliximab (Remicade)
Adalimumab (Humira)
Golimumab (Simponi)
Certolizumab (Cimzia)
143
Q

Clinical use of TNF antagonists (biologics) in RA

A
  • rapid response times, very effective
  • best when combined with MTX
  • all pts should be screened for latent TB
144
Q

Drugs used in RA to put pts into remission and keep them there

A

DMARDs and biologics

-but need NSAIDs and CSs in mean time to control disease in the meantime

145
Q

Guidelines for using CSs in RA:

A

Start DMARDs ASAP - most important, will slow progression of disease and put them into remission

Use CSs as a bridge to effective DMARD therapy (1-3months)

146
Q

Oral CS dose for RA

A

Less than 10mg a day usually needed

147
Q

Initial drug treatment for RA

A

NSAIDs

  • but does NOT slow progression
  • usually started until can see rheumatologist, and then put on DMARD and they either leave NSAID on or switch it out for CS for 3 months until DMARD works
148
Q

3 main types of juvenile RA

A

Systemic
Polyarticular
Pauciarticular

Classified by the sx in the first 6 months

149
Q

JRA definition

A

Persistent arthritis in 1 or more joints for at least 6 weeks

150
Q

Systemic JRA

A

Fever, rash, myalgia, organomegaly + arthritis

-more severe in presentation

151
Q

Polyarticular JRA

A

Symmetric arthritis involving large and small joints

152
Q

Pauciarticular JRA

A

Less joints affected, but usually the larger joints

-asymmetric

153
Q

Most likely type of JRA to go into remission

A

Systemic

-even though most severe initial presentation

154
Q

JRA tx

A
  • more joints effected = DMARD
  • less joints effected = intra-articulate CS injection, oral NSAIDs

PT/OT is big

155
Q

Major Findings in Salicylate Toxicity

A
  • resp alkalosis
  • resp acidosis
  • metabolic acidosis
  • fluid/electrolyte imbalances
  • hypoglycemia
  • mental status change
156
Q

Salicylate nomogram

A

Dome nomogram

-role in late presentation - extrapolate backwards

157
Q

How often to measure Salicylate serum levels and pH in OD

A

Q2h

Why do we care about pH? If pH is low, Salicylate could be hiding out in the tissues and can end up redistributing

158
Q

Mainstay of treatment for Salicylate toxicity

A

Alkalinization (increase pH)

  • give sodium bicarb, but not in CHF pt
  • would use HD in CHF pts
159
Q

Most toxic NSAIDs

A

Phenylbutazone and mefenaic acid

-both enolic acids

160
Q

Management of toxicity in NSAIDs

A

Sx and supportive care - milk

161
Q

Antidote for NSAID and Salicylate toxicity?

A

No

162
Q

Pathophysiology of Parkinsons Disease

A

Gradual destruction of neurons from substantia nigra to the striatum of brain that use dopamine to communicate (responsible for movements)

163
Q

Sx of parkinsons are characteristic of

A

Decreased dopamine

164
Q

Dopamine is a precursor to….

A

NE and E

-explains some other sx

165
Q

Classic Parkinsons Features

A

Tremor
Bradykinesia
Rigidity

166
Q

Dont see classic features of parkinsons until….

A

60-80% of neurons have been destroyed and cant get back

167
Q

Other features of parkinsons

A
  • difficulty concentrating
  • change is sense of smell
  • constipation
  • mood change
  • difficulty swallowing, speaking, blinking
168
Q

Big part of parkinsons care

A

Multi-disciplinary care

OT, PT, speech therapist

169
Q

Limitation to tx for parkinsons

A

Doesnt affect disease process, nothing stops neuron destruction

QOL only

170
Q

Cornerstone of therapy for parkinsons

A

Levodopa

171
Q

Levodopa MOA

A

Levodopa is a prodrug that DOES cross BBB and gets converted to dopamine
-needs to be paired always with a decarboxylase inhibitor (carbidopa or benserazide) that DOES NOT cross BBB so that this conversion of dopamine isnt happening in the periphery and mostly just in BBB

172
Q

Dopamine Agonists used in parkinsons

A 
Bromocriptine 
Pramipexole
Ropinorol
Rotigotine 
Apomorphine - new IV for acute tx (if in distress)
173
Q

Dopamine Agonists use in Parkinsons

A

Alone or in addition to levodopa

-could be used alone to save levodopa for later

174
Q

AE of dopamine agonists in parkinsons

A

Poor impulse control - gambling, hypersexuality

175
Q

MAO-B Inhibitors used in Parkinsons

A

Selegine

Rasagiline

176
Q

Downside of MAO-B inhibitors in parkinsons

A

Have to avoid tyramine containing foods

-beer, red wine, cured/smoked meats, cheese

177
Q

Amantadine role in parkinsons

A

Add-on only

-effects only last 3-4 months so have to use cycle dosing

178
Q

COMT Inhibitors used in Parkinsons

A

Entacapone

Tolcapone

179
Q

COMT Inhibitors role in Parkinsons

A

Has to be used with levodopa - no effect if given alone!!

  • specifically used for “wearing off” effect of levodopa
  • decrease levodopa dose by 30% when starting
180
Q

Anticholinergics used in parkinsons

A

Benztropine
Ethopropazine
Trihexyphenidyl

181
Q

Anticholinergics role in Parkinsons

A

Only treats tremor!

-caution in elderly

182
Q

Supportive meds used in parkinsons

A 
Sleep aids
Antidepressants 
Laxatives
Eye lubricant
Antemetics
183
Q

What to do if levodopa is failing?

A
  • decrease protein in diet
  • change to CR @ HS
  • smaller, more frequent doses
  • add another agent
184
Q

All parkinsons agents usually cause…

A

Hypotension

185
Q

A systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk

A

Osteoporosis

186
Q

Osteoporosis T-score definition

A

T-score greater than or equal to 2.5 SD below the peak mean

187
Q

2 types of bone

A

Cortical and cancellous

188
Q

Osteoblasts

A

Bone builders

189
Q

Osteoclasts

A

Resorp bone

-transfer Ca out of bone, into blood stream

190
Q

Osteocytes

A

Regulate rate of bone mineralization

191
Q

Hormones involved in bone resorption

A

Parathyroid hormone

Glucocorticoid hormones

192
Q

Hormones involved in bone formation

A

Estrogens, testosterone, calcitonin

193
Q

At what age is there a decrease in cortical bone

A

35yrs

-speeds up during menopause period as well

194
Q

3 types of OP

A
  1. Post-menopausal
  2. Senile - over age 75yrs
  3. Secondary
195
Q

Weight-bearing exercise is good in…

A

OP

  • not swimming or biking
  • goal is 30-45mins 3-4x per week
196
Q

Lifestyle factors increasing risk of OP

A

Alcohol - intoxicates osteoblasts
Smoking - inhibits estrogen
Caffeine

197
Q

Greatest risk than other fx sites

A

Hip and vertebrae

198
Q

OP physical exam

A 
Weight loss?
Height loss?
Rib to pelvis?
Occupit to wall?
Get up and go risk
199
Q

T-score is used for….

A

Adults 50 and over

200
Q

Z-score is used for…

A

Adults younger than 50

-can dx OP by BMD for adults younger than 50

201
Q

Calcium requirement for those over 50yrs

A

1200mg/day elemental

  • calcium carbonate = 40%
  • calcium citrate = 21%
  • calcium gluconate = 9%
202
Q

Vit D recommendation for OP

A

800-2000 IU daily
(20-50mcg)

Aids in calcium absorption
D3 cholecalciferol preferred

203
Q

Other anti-resorptives used in OP

A

Raloxifene
Hormone therapy
Calcitonin
Denosumab

204
Q

Bisphosphonate MOA

A

Inhibits osteoclast activity

205
Q

Extremely poor _____ of bisphosphonates in OA

A

Bioavailability

-so adherence is very important for efficacy!

206
Q

Bisphosphonate of use if wanting to become pregnant

A

Risedronate - shorter half-life

-give women the info and options

207
Q

Bisphosphonate dosing

A

Options for daily, weekly, or monthly (with ER risedronate)

208
Q

How to take bisphosphonate

A

Take on empty stomach and with lots of water

Stay upright for 30mins and wait 30mins before first food intake

Would take ER risedronate with food

209
Q

Bisphosphonate that is IV

A

Zoledronic acid given once a year

210
Q

Raloxifene in OP

A

SERM - selective estrogen receptor modulator

First-line for menopausal women to prevent vertebral fx

211
Q

When to use hormone therapy in OP

A

Only in postmenopausal women requiring tx of OP in COMBO with tx of vasomotor sx

212
Q

Risk of using hormonal therapy for OP

A

Endometrial cancer
Breast cancer
Thromboembolic disease
CHD

213
Q

Teriparatide (Forteo) in OP

A

Increases osteoblast activity - different than all other ones for OP as it doesnt prevent bone breakdown, but builds it up

PHARM 557 (3 decks)

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