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Therapeutics 4 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Urate

A

Ionized form of uric acid

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2
Q

Hyperuricemia

A

serum urate concentration >6.8mg/dL

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3
Q

Gout

A

Monosodium urate (MSU) crystals in joints, bones, and soft tissue

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4
Q

What do you think of when you think of gout?

A

Uric acid

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5
Q

Causes of gout

A

Overproduction (10%)

Underexcretion (90%)

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6
Q

Risk factors for gout

A

Male and postmenopausal females, age, obesity, alcoholism, dehydration, excess cell turnover, genetic conditions, hyperuricemia, hypothyroidism, medications, renal impairment, sex, trauma

Think about kidney dysfunction! Age and obesity can affect this.

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7
Q

Causes of overproduction of uric acid

A

Dietary purine- meat, seafood, beer
Endogenous purine synthesis- malignancy, tumor lysis syndrome
Purine salvage- enzyme deficiency
Purine breakdown- glycogen storage disease

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8
Q

Causes of underexcretion of uric acid

A

Urinary excretion- diuretics (thiazides, dose dependent), renal failure
Urinary reabsorption- alcohol, genetic defects

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9
Q

Why might we limit purine in gout?

A

Purine is metabolized by xanthine oxidase and turned into uric acid.

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10
Q

Acute gout

A

Uric acid crystal formation
Crystal deposits in joint
Phagocytosis of crystals leads to proinflammatory cytokine release.
Acute attacks will self-terminate but we often treat because of s/s

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11
Q

What to think of when you think about osteoarthritis?

A

Cartilage

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12
Q

Is OA inflammatory?

A

No

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13
Q

OA pathophysiology

A

Cartilage repair problem
Can be because of- bone cyst, thickened joint capsule, synovial inflammation, cartilage fibrillation, meniscal degeneration, osteophyte formation, subchondral bone releases MMPs, bone marrow lesion, joint space narrowing.

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14
Q

Risk factors of OA

A

Age, genetics, weight, environmental/repetitive use (sports, factory, construction, trauma), family history, previous joint injury, female

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15
Q

What to think of when you think of RA

A

Broad spectrum very aggressive inflammation

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16
Q

What is the cause of RA?

A

Unknown
Could be because of bacteria, genetics, smoking, other
Something causes abnormal IgG antibody development and the development of rheumatoid factor (an antibody) against the IgG antibodies.
RF forms a complex that leads to inflammation which can lead to cartilage damage.
The complement system is then activated which attracts leukocytes and stimulates inflammatory mediator release

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17
Q

HLA-DR 4

A

If this is positive, you are more likely to have RA

It is a genetic receptor on cells that stimulate immune response

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18
Q

Risk factors of RA

A

Age (30s-40s), female, genetics, obesity, tobacco use (linked to poor prognosis)
HLA-DR4 positive

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19
Q

Can human convert urate to allantoin?

A

No, humans lack uricase

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20
Q

Does gout need hyperuricemia?

A

No

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21
Q

Hyperuricemia range in men and women

A

> 7 in men, >6 in women

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22
Q

Does hyperuricemia= gout?

A

No

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23
Q

Medications that increase uric acid levels

A

Cytotoxic agents, cyclosporine, diuretics (thiazides), levodopa, nicotinic acid, salicylates (<2g/day)

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24
Q

Diagnosis of gout- EULAR 2018

A

1.) When possible, identify monosodium urate (MSU) crystals in the synovial fluid. This is painful and most patients will not allow.

  1. ) If not possible, clinical diagnosis based on clinical features and presence of hyperuricemia.
    - MTP or ankle joint, previous gout, rapid onset, erythema, male gender, CV disease

3.) If diagnosis is uncertain, use imaging/ultrasound to look for crystal deposits

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25
Q

Diagnostic testing with gout

A

CBC, SCr, Serum uric acid

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26
Q

Acute gout attack symptom presentation

A

Affected joints- first metarsophalangeal joint, joints in fingers, wrist, or feet, monoarthritis in beginning

S/S- erythema, fever, intense pain, joint inflammation, swelling, warmth

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27
Q

Non pharm management of gout

A

Apply ice, dietary changes (avoid/minimize alcohol, purine rich foods, high fructose corn syrup), weight management (lose weight if needed)

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28
Q

Gout concurrent medication considerations

A

Conditional recommendation- change HCTZ to another antihypertensive agent, losartan preffered
Conditionally recommend against stopping low dose aspirin, changing cholesterol tx to fenofibrate

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29
Q

Acute gout treatment options

A

Colchicine, NSAIDs, glucocorticoids are 1st line

IL-1 inhibitors rarely used

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30
Q

Colchicine

A

Low dose colchicine is preferred over high dose due to similar efficacy and lower risk of AE.
Gout

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31
Q

Contraindications of colchicine use

A

Hypersensitivity
Renal and hepatic impairment
Renal or hepatic impairment and taking either a P-glycoprotein inhibitor or a strong CYP3A4 inhibitor

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32
Q

Colchicine AE

A

GI, elevated hepatic enzymes, myopathy, neutropenia, thrombocytopenia

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33
Q

Onset of action for colchicine

A

12 hours

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34
Q

Colchicine prophylaxis dose

A

0.6 mg QD to BID

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35
Q

Colchicine acute flare management

A

1.2 mg x 1 followed by 0.6 mg one hour later. May repeat no earlier than 3 days

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36
Q

Colchicine dosing with strong CYP3A4 inhibitors

A

Clarithromycin, protease inhibitors, ketoconazole

0.6mg x 1 followed by 0.3 mg one hour later

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37
Q

Colchicine dosing with moderate CYP3A4 inhibitors

A

Diltiazem, fluconazole, grapefruit juice, verapamil

1.2 mg x 1- may repeat no earlier than 3 days later.

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38
Q

Colchicine with P-glycoprotein inhibitors dosing

A

Cyclosporine, ranolazine- 0.6mg x 1- do not use earlier than 3 days later

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39
Q

Colchicine in CrCl <30 or severe hepatic impairment

A

May repeat no earlier than 2 weeks

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40
Q

Does colchicine help improve CV outcomes?

A

Yes

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41
Q

NSAID BBW

A

CV risk, GI risk

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42
Q

NSAID precautions

A

Alcoholism, anemia, anticoagulant therapy, aspirin sensitive asthma, breastfeeding, heart disease, hepatic disease, kidney disease, peptic ulcer disease, pregnancy >20 weeks, steroid therapy

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43
Q

NSAIDs for gout

A

Celecoxib: 800mg x 1 followed by 400mg on day 1; then 400mg BID for 1 week
Ibuprofin: 400-800 mg TID-QID
Indomethacin 50 mg TID
Meloxicam 7.5-15 mg QD
Naproxen 750 mg x 1 and then 250 mg q 8 h until attack subsides

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44
Q

Contraindications to corticosteroids

A

Hypersensitivity
Serious infection
Systemic fungal infection

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45
Q

Prednisone AE

A

Glucose intolerance, insomnia, increased appetite, agitation, BP elevation, predisposition in infections

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46
Q

Prednisone DDI

A 
NSAIDs- increase risk of ulceration
Variable effects on warfarin
Cyclosporine
Live vaccines
Immunosuppressants
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47
Q

Corticosteroid dosing for gout

A

Prednisone- 30-60 mg QD x 3-5 days, then taper by decreasing 5 mg/day
IM triamcinolone- 60 mg x 1 followed by prednisone
Intra-articular- triamcinolone 10-40 mg (large joints) or 5-20 mg (small joints) in combo with 1 of the acute treatment agents

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48
Q

IL-1 inhibitors for gout

A

Anakinra- 100 mg SC QD for 3 days

Canakinumab- 150 mg SC QD

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49
Q

Who should receive urate lowering therapy?

A

Strongly recommend if >1 tophus, evidence of radiographic damage attributable to gout, > 2 gout attacks per year
Conditionally recommend if previously experienced >1 flare but have infrequent flares (<2 per year) or experiencing first flare and CKD stage >3, serum uric acid >9

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50
Q

ACP

A

Gout guideline

Treat to avoid symptoms with no uric acid level monitoring

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51
Q

ACR

A

Gout guideline

Serum urate concentration <6 mg/dL

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52
Q

Tophaceous gout

A

Tophi= urate deposits

Complications- deformity, joint destruction, nerve compression, pain

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53
Q

Kidney impact of gout

A

Uric acid kidney stones
Acute uric acid nephropathy
Chronic uric acid nephropathy

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54
Q

What urate lowering therapy is recommended?

A

Allopurinol is preferred as first line

Allopurinol or febuxostat stronglt recommended over probenecid for patients with moderate to severe CKD

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55
Q

Gout anti-inflammatory prophylaxis

A

Strongly recommend initiation of concurrent anti-inflammatory prophylaxis (colchicine, NSAID, prednisone) x 3-6 months over no anti inflammatory prophylaxis

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56
Q

Urate lowering therapy (ULT) options

A

Xanthine oxidase inhibitors (XOI)= allopurinol and febuxostat
Uricosurics- probenecid, Lesinuraf + XOI

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57
Q

AE of XOI

A 
N/V
Bone marrow suppression (allopurinol)
Acute arthritis attack
Arthralgia
Cardiac adverse events (febuxostat)
Skin rash
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58
Q

Allopurinol and didanosine DDI

A

Pancreatitis risk

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59
Q

Can you use febuxostat in hepatic impairment?

A

Unknown, has not been studied

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60
Q

Febuxostat DDI

A

Azathioprine, mercaptopurine

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61
Q

Allopurinol hypersensitivity syndrome risk

A

Female, 60 years or older, initiation dose >100 mg /day, kidney disease, CV disease, use of allopurinol for asymptomatic hyperuricemia, HLA-B *5701 allele

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62
Q

XOI DDI

A

Azathioprine, mercaptopurine- metabolized by xanthine oxidase
ACEI, thiazides- may predispose patients to hypersensitivity rxn w/ allopurinol
Capecitabine
Pegloticase

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63
Q

Allopurinol dosing

A

Start at <100mg/day. If CKD stage 3 or 4, start at 50/day
100-300mg daily or every other day (max 800mg/day)
Titrate q 2-5 weeks prn

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64
Q

Febuxostat BBW

A

Risk of CV death

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65
Q

Febuxostat dosing

A

Begin at 40 mg daily

May increase to 80 mg daily after 2 weeks

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66
Q

Probenecid (uricosuric) contraindications

A 
Hypersensitivity to drug or sulfonamides
Aspirin
Bone marrow suppression
Children <2 years old
Renal impairment 
H/O renal uric acid stones
Uric acid overproducers
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67
Q

Probenecid AE

A

Bone marrow suppression, GI, precipitation of acute arthritis attack, stone formation

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68
Q

Probenecid DDI

A

Increases concentrations of ketorolac and methotrexate

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69
Q

Probenecid dosing

A

250 mg BID x 1-2 weeks; then, 500 mg BID

Give plenty of fluids

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70
Q

Lesinurad

A

Add-on uricosuric to XOI

For patients not reaching target serum uric acid levels with XOI

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71
Q

Lesinurad contraindications

A

Severe hepatic impairment
CrCl <45
ESRD, kidney transplant, dialysis
Secondary hyperuricemia

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72
Q

Lesinurad DDI

A

CYP2C9 substrate, weak CYP3A4 inducer, hormonal contraceptive, increases nisoldipine, valproic acid

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73
Q

Lesinurad AE

A

HA, increased creatinine levels, GERD, possible increased risk of CV events

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74
Q

Lesinurad dosing

A

200 mg PO QAM with food and water

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75
Q

Pegloticase

A

Use if XOI treatment and uricosurics have failed to achieve optimum serum uric acid target.
MOA: recombinant uricase enzyme. Increases conversion of uric acid to allantoin.

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76
Q

Pegloticase BBW

A

Only in specialized treatment facilities

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77
Q

Pegloticase contraindication

A

G6PD deficiency

Caution in HF

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78
Q

Types of arthritis

A

Gouty arthritis
Osteoarthritis
Rheumatoid arthritis

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79
Q

Inflammatory mediators in RA

A

IL-6, TNFa, prostaglandins

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80
Q

Drug therapy for RA

A

Mild- NSAIDs

Moderate to severe= DMARDs

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81
Q

DMARDs

A

Disease modifying AntiRheumatic Drug
Slow down progression of disease= disease-modifying
Not a reduction of symptoms alone

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82
Q

DMARDs include

A

Etanercept, Infliximab, Adalimumab, Anakinra

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83
Q

Immune signaling in arthritis

A

IL-1 signaling, JAKSTAT signaling, TNF alpha signaling

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84
Q

Entanercept

A

Recombinant form of soluble human TNF receptor linked to IgG1
MOA- soluble protein binds to TNF-alpha inhibiting its action at endogenous receptor.
Long acting injection

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85
Q

Entanercept AE

A

significant immunosuppression, can result in neuronal demyelination (rare), increased risk of lymphoma, hepatitis B reactivation

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86
Q

Infliximab and Adalimumab

A

Same MOA as entanercept
Different version of humanized antibodies that bind to TNF alpha
AE- immunosuppression

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87
Q

Certolizumab

A

Humanized Fab’ fragment- PEG linked
PEG fragment increases plasma 1/2 life
Neutralizes membrane-associated and soluble human TNF alpha

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88
Q

Golimumab

A

Neutralizes membrane associated and soluble human TNF-a
subq injection once monthly
Used for RA WITH methotrexate

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89
Q

Anti-metabolites

A

Act to halt cell growth or division

Most interfere with the cellular machinery required for these processes

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90
Q

Methotrexate

A

Suppresses the proliferation of immune cells.
Inhibits dihydrofolate reductase (DHFR)
Inhibits neutrophils and T cells and results in B cell reduction

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91
Q

Methotrexate ADME

A

A- readily absorbed in GI tract
D- slow, CNS
M- minimal metabolism
E- renal

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92
Q

Leflunomide

A 
Pyrimidine synthesis inhibitor
Inhibits dihydroorotate dehydrogenase 
Used for RA
AE- liver damage, immunosuppression
BBW- pregnancy
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93
Q

Colchicine MOA

A

antimitotic effects, arrests cells in G1 phase

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94
Q

Probenecid moa

A

Organic anion transporter (OAT) inhibitor. inhibits the reuptake of uric acid from urine to blood.

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95
Q

Probenecid ADME

A

A- complete orally
D= plasma protein bound
M- dose dependent, 5-8 h
E- kidney

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96
Q

5 steroid classes

A 
Progestogens
Glucocorticoids
Mineralcorticoids
Androgens
Estrogens
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97
Q

Progestogens

A

Pregnancy maintenance

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98
Q

Glucocorticoids

A

Gluconeogenesis and glycogen formation, inflammatory response inhibition.

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99
Q

Mineralcorticoids

A

Salt and water balance, modulate BP and volume

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100
Q

What are steroids derived from?

A

Cholesterol

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101
Q

Steroid MOA

A

Bind to cytosolic intracellular receptors which enter the nucleus.
Hormone receptor heterodimer acts as a transcription factor and alters gene expression.

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102
Q

physiologic corticosteroid regulation

A 
Exogenous glucocorticoids (prednisone) inhibit the release of corticotropin releasing hormone (CRH) and adrenocorticotropic hormone (ACTH)
Leads to symptoms of addisons disease (primary adrenal insufficiency)
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103
Q

Hydrocortisone

A

Exogenous cortisol acts to alter immune system function and inhibit inflammation.
MOA- regulation of glucocorticoid receptor and gene transcription

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104
Q

Excessive corticosteroid AE

A

Cushings disease

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105
Q

Corticosteroids dose tapering

A

All corticosteroids require gradual dose reductions
Can have rebound effect (steroid withdrawal syndrome)
Tapering can take months or years

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106
Q

Corticosteroid therapy length

A

Lowest doses should be utilized
Short term therapy- tapered over 1-2 weeks
Long term therapy= months to years

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107
Q

Osteoarthritis definition

A

OA affects primarily the weight-bearing joints, causing pain, limitation of motion, deformity, progressive disability and decreased quality of life. It is characterized by increased cartilage destruction and subsequent proliferation of adjacent bone.

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108
Q

How is joint distribution different for OA compared to gout?

A

OA- hip, hand, knee, spine, feet

Gout- big toe, 1 joint space, peripheral

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109
Q

Primary/idiopathic OA vs secondary OA

A

Primary/idiopathic- generalized or localized. Has about a 30% genetic component.
Secondary- Congenital factor, inflammatory arthritis, metabolic r endocrine disorder, trauma

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110
Q

Compare and contract the risk factor for gout and OA

A

Both- age, trauma, overweight, FH
Gout- males
OA- females, recreational activity

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111
Q

Gout diagnosis

A

History, physical exam, lab parameters (ESR and RF negative), Radiographic findings (joint space narrowing, osteophytes, subchondral sclerosis)

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112
Q

Presentation of OA

A

Symptoms limited to involved joints (weight bearing joints, 1 or fewer)
Joint pain most common symptom. Pain on motion and relieved by rest.
Joint- tenderness, instability, deformity
Osteophyte formation
Morning joint stiffness

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113
Q

OA Physical exam

A

Decreased range of motion

Typically joints do NOT have erythema, heat, large effusions, extreme tenderness to palpation

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114
Q

OA in hands

A 
Heberdons Node (at distal interphalangeal joint)
Bouchards Node- at proximal interphalangeal joint
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115
Q

WOMAC pain severity

A

Used for RA
Hip and knee
24 items, 5 point likert scale
Stiffness, pain, effect on daily activities/physical function

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116
Q

Non pharm recommendations for hand OA

A

Exercise, self-efficacy and management programs, 1st CMC orthosis

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117
Q

Non pharm for knee OA

A

Exercise, self efficacy and management, weight loss, Tai Chi, Cane, TF Knee brace

118
Q

Non pharm for hip OA

A

Exercise, self-efficacy and management programs, weight loss, tai chi, cane

119
Q

Pharmacologic recommendations for hand OA

A

Oral NSAIDs only think strongly recommended

Can use other agents- topical NSAIDs, I-A steroids, APAP, tramadol, duloxetine, chondroitin

120
Q

Pharmacologic recommendations for knee OA

A

Oral NSAIDs, topical NSAIDs, I-A steroids

121
Q

Hip pharmacologic recommendations for OA

A

Oral NSAIDs, imaging guidance

122
Q

Oral NSAIDs for OA

A

Celecoxib- 100 mg BID or 200 mg QD
Ibuprofen 400-800 mg TID-QID
Naproxen 250-500mg BID

123
Q

Diclofenac gel for OA

A

Smaller joints (hand, knee)- dose 2 or 4 grams or no more than 2 joints QID (max 32 grams/day)

124
Q

Diclofenac gel administration

A

Wash hands before/after application
Do not wash hand for 1 hour after application to hand
Do not shower for 1 hour after application
Do not apply to open wounds
Do not use occlusion or heat on application site. Do not cover with clothes for 10 minutes after application.
Minimize sun exposure after application

125
Q

Intra-articular steroids in OA

A

May be a placebo effect
Intra-articular triamcinolone 5-40 mg q 3 months, depending on formulation
Onset of pain relief- 1-2 days lasts for 1 month
Dose q 3 months

126
Q

APAP in OA

A

1 gram QID

Not as effective as NSAIDs

127
Q

Tramadol in OA

A

Used in moderate-severe pain before stronger opioids
IR- 24-50 mg q 6 h prn
ER- 100mg/day
May cause seizures

128
Q

Duloxetine in OA

A

30 mg QD for 1 week and then, increase to 60 mg QD

AE- N, dry mouth, falls, fatigue, drowsiness

129
Q

Chondroitin in OA

A

Modest efficacy
800-2000 mg/ day (QD or divided doses)
SE- GI

130
Q

Topical capsaicin in OA

A

Apply a thin layer of cream TID-QID
Delayed onset
Burning, stinging possible

131
Q

What should you NOT use in OA?

A

Biphosphonates, glucosamine, hydroxychloroquine, methotrexate, TNF inhibitors, IL-1 ra

132
Q

Multifactorial care in OA

A

Depression, fall risk minimization, occupational maintenance, recreational activity maintenance, sleep, stress management

133
Q

RA guideline

A

American college of rheumatology

134
Q

RA definition

A

RA is a common, chronic, progressive autoimmune condition that primary affects the joint and synovium but can also have detrimental effects on organ systems throughout the body

135
Q

What has a protective effect on RA?

A

Omega-3 rich diet (>3 g/day)

Testosterone

136
Q

Clinical presentation of RA

A 
Hands, wrists, ankles, feet (multiple joint involvement)
Symmetry (very important!)
Warmth and swelling
Joint stiffness in morning > 30 minutes
Decreased function
Symptoms for 6+ weeks
137
Q

Labs for RA

A 
Rheumatoid factor +
Anti-cyclic citrullinated antibodies
Erythrocyte sedimentation rate +
C-Reactive protein +
Synovial fluid analysis- WBC, but no bacteria
138
Q

Clinical involvement- X rays RA

A 
Joint space narrowing
Joint subluxation
Joint deviation
Bony erosions
Periarticular osteopenia
139
Q

Clinical presentation of RA- extra articular involvement

A 
Generalized fatigue and weakness
Rheumatoid nodules
Interstitial lung disease
Vasculitis
Sjorgens syndroms
Pericarditis
Felty syndrome
Coronary artery disease
Ocular manifestations
140
Q

Diagnosis of RA

A

Earlier diagnosis of patients with RA allows for earlier treatment to prevent joint damage
There is a scoring system that assigns points based on the number and types of joints involved. A score of 6 or m ore is diagnostic of RA

141
Q

How often should treatment of RA be reevaluated?

A

At least every 3 months

142
Q

Treatment of RA

A

csDMARDs- hydroxychloroquine, sulfasalazine, methotrexate, leflunomide
bDMARDs- TNF inhibitors, IL-6 inhibitors
tsDMARDs- JAK inhibitors

143
Q

Synthetic DMARDS

A

csDMARDs- methotrexate, leflunomide, sulfasalazine, hydroxychloroquine
Targeted synthetic DMARDs- baricitinib, tofacitinib, upadacitinib

144
Q

Biologic DMARDs

A

TNFi- adalimumab, certolizumab, etanercept, golimumab, infliximab
IL-6Ri- sarilumab, tocilizumab
Costimulation-I- abatacept
Anti-B cell- rituximab

145
Q

Biosimilar DMARDs

A

For adalimumab, etanercept, infliximab, rituximab

146
Q

Are biosimilars considered equivalent to FDA approved bDMARDs?

A

Yes

147
Q

Serious infection

A

an infection requiring IV abx or hospitalization

148
Q

Triple therapy in RA

A

Hydroxychloroquine, sulfasalazine, and either methotrexate or leflunomide

149
Q

Treat to target in RA

A

Refers to the systematic approach involving frequent monitoring of disease activity using validated instruments and modification of treatment to minimize disease activity with the goal of reaching a predefined target (low disease activity or remission)

150
Q

Recommendations referring to bDMARDS exclude what

A

rituximab unless pts have had an inadequate response to TNF inhibitors of have a history of lymphoproliferative disorder

151
Q

Disease Activity Score (DAS28)

A

Scale 0-9.4
Remission <2.6
Low disease activity: 2.6-3.2
High disease activity >5.1

RA assessment tool

152
Q

DMARD-Naive patients with moderate to high disease activity tx- RA

A

Methotrexate strongly recommended over hydroxychloroquine or sulfasalazine, bDMARD, or tsDMARD monotherapy
Methotrexate plus a non TNF inhibitor bDMARD or ts DMARD

153
Q

Should you initiate csDMARD with or without long or short term glucocorticoids for DMARD naive patients?

A

Without

154
Q

Recommendations for csDMARD treated, but MTX naive patients with moderate to high RA disease activity

A

Methotrexate monotherapy is recommended over combination of MTX plus a bDMARD or tsDMARD

155
Q

DMARD naive patients with low disease activity recommendations

A

Hydroxychloroquine recommended over other csDMARDS
Sulfasalazine recommended over MTX
MTX recommended over leflunomide

156
Q

MTX initiation recommendations

A

Titrate to a weekly dose of at least 15 mg within 4-6 hours

157
Q

Target for RA?

A

Remission

158
Q

What tx approach is recommended in RA?

A

Treat to target approach

159
Q

Nonpharm for RA

A

Assistive devices, heat, mental health resources, occupational therapy, patient education, physical activity, physical therapy, weight loss, rest (limited)

160
Q

RA ACR suggested baseline evaluation

A

CBC, creatinine, CRP, ESR< LFTs, BMP, stool guaiac, synovial fluid, urinalysis
Radiography, ultrasonography, or magnetic resonance imaging of affected joint

161
Q

Live vaccines

A 
Adenovirus
BCG
Measles, mumps
Oral polio
Oral typhoid
Rubella
Smallpox
Varicella
Yellow fever
162
Q

How long do you have to avoid live vaccines after steroids?

A

Live vaccines should be avoided for at least 1 month after completing high dose systemic steroid therapy (pred >20mg/day for > 14 days)

163
Q

Methotrexate BBW

A 
Pregnancy and breastfeeding (avoid pregnancy for 6 months after last dose, m/f)
Ascites
Bone marrow suppression
Diarrhea
Exfoliative dermatitis
Hepatic disease
Infection
Intraeuterine fetal death
Lymphoma
Pleural effusion
Pulmonary disease
Radiation therapy
Renal impairment
Requires an experienced clinician
Stomatitis
Tumor lysis syndrome
164
Q

Methotrexate monitoring

A

AST, ALT, Alk phos- hepatotoxicity
CBC- bone marrow suppression
SCr- kidney function

165
Q

Methotrexate contraindications

A

Pregnancy/ breastfeeding
Alcoholism
Bone marrow suppression/immunodeficiency
Hepatic disease

166
Q

Methotrexate AE

A

GI (N/D), alopecia, hematologic, pulmonary, hepatic, stomatitis, folic acid deficiency

167
Q

MTX DDI

A 
NSAIDs- increase MTX concentrations
Trimethoprim/Bactrim- increase BMS
leflunomide- increased hepatotoxicity
Highly protein bound drugs- increase MTX conc
Probenecid- increase MTX conc
High dose ASA- increase MTX conc
PPIs- decrease renal elimination
168
Q

Methotrexate dose

A

7.5-15 mg/ week
7.5 mg/week to start
Add folic acid 1 mg daily

Max 25 mg/week

169
Q

Methotrexate monitoring

A

Watch for mouth ulcers, SOB, new onset cough, N/D, s/s of immunosuppression, pregnancy
Need labs before therapy

170
Q

Leflunomide contraindications

A

Liver disease (BBW)
Pregnancy/breastfeeding (BBW)
Men wanting to father children

171
Q

Washout protocol for leflunomide

A

Cholestyramine 8g TID x 11 days

Level must be <0.002mcg/mL (if not, repeat)

172
Q

Leflunomide AE

A 
GI (D)
Hepatotoxicity
Alopecia
HTN
Bone marrow toxicity
Peripheral neuropathy
Skin rash
173
Q

Leflunomide DDI

A

Moderate CYP2C9 inhibitor

  • hepatotoxins
  • Live vaccines
  • Rosuvastatin, possible other statin
  • Uricosurics
174
Q

Leflunomide dose

A

10mg QD x 3 days followed by 20 mg QD or 10-20 mg QD without LD

175
Q

Monitoring of leflunomide

A

Diarrhea, weight loss, N/V, pregnancy

Same labs as MTX

176
Q

Hydroxychloroquine contraindications

A

Hypersensitivity, visual changes due to 4-aminoquinoloines, pre-existing ocular disease, G6PD deficiency

177
Q

Hydroxychloroquine DDI

A

CYP2D6 inhibitor, decreased by antacids
QT prolonging drugs
Increases cyclosporine

178
Q

Hydroxychloroquine dose

A

200 mg BID or 400 mg QD with food

Do not exceed 5mg/kg/day or 400 mg daily

179
Q

Hydroxychloroquine monitoring

A

Visual changes, eye exams

180
Q

Sulfasalazine dose

A

500 mg QD-BID titrated to 1000 mg BID

181
Q

Sulfasalazine monitoring

A

watch for immunosuppression, photosensitivity, rash, GI
CBC
Consider G6PD evaluation at baseline
Caution use in hepatic or renal impairment

182
Q

What to do prior to giving biological DMARDs

A

Prior to starting therapy, give tuberculin skin test, hepatitis B screen, assess infection risk
Drug interactions- live vaccines, other biologics

183
Q

Is there added efficacy to being on 2 biologics?

A

No, just an increased risk of infection

184
Q

TNF inhibitors

A 
Etanercept
Infliximab
Adalimumab
Certolizumab
Golimumab
185
Q

Which TNFi are available IV?

A

Infliximab- IV only

Golimumab- IV and SC

186
Q

Which TNFi increase risk of upper respiratory tract infections?

A

Certolizumab, golimumab

187
Q

AE of infliximab

A

infusion-related reactions, HA, abdominal pain, antibody formatin

188
Q

AE of certolizumab

A

Upper respiratory tract infection, rash, UTI

189
Q

TNFi BBW

A

Infection, malignancy risk

Certolizumab- children

190
Q

TNFi absolute contraindications

A

Sepsis

Murine protein hypersensitivity (infliximab)

191
Q

Is infliximab always used with MTX?

A

yes

192
Q

TNFi precautions

A

HF, demyelinating disorders, risk for pancytopenia, lupus-like reaction, immunosuppression, hepatotoxicity, COPD

193
Q

TNFi DDI

A

Contraindicated- other TNF inhibitors, live vaccines, rilonacept
Avoid other biologic therapies

194
Q

TNFi monitoring

A 
S/S infection
S/S of CHF or demyelinating disease
Tuberculin skin test
CBC
LFTs
195
Q

Abatacept, what is it? warnings?

A

Non-TNFi (only use if pt has failed TNFi)
Warnings- anaphylaxis, COPD, infection, malignancy risk
contraindications- hypersensitivity to abatacept or maltose

196
Q

Abatacept AE

A

HA, upper respiratory infection, nausea, drug infusion reaction, serious infection

197
Q

How is abatacept given?

A

IV or SC

198
Q

IL-6 inhibitors BBW and contraindications

A

BBW- infection (check tuberculosis prior to starting)

Contraindications- not recommended for initiation, need to dose modify or dc if abnormal LFTs, ANC, or platelet count

199
Q

IL-6 monitoring

A

ANC, LFTs, platelet count, lipids, neutrophils

200
Q

IL-6 AE

A

Infection, BP changes, increased ALT, lipid changes, lower intestinal perforation, malignancy

201
Q

IL-6 DDi

A 
Live vaccines
other biologics
drugs metabolized by CYP3A4
Simvastatin
Cyclosporine
202
Q

IL-6 inihbitor agents

A

Tocilizumab- SC and IV

Sarilumab- SC

203
Q

JAK inhibitors BBW

A

Infection, new primary malignancy, thromboembolism, mortality

204
Q

Jak inhibitors warnings

A

Do not start if lymphocyte <500 or if ANC <1000 or hemoglobin <9
GI perforation
Renal disease

205
Q

JAK inhibitor AE

A

Infection, thrombosis, lipids, LFTs elevation, neutropenia, anemia

206
Q

JAK inhibitor agents

A

Baricitinib, tofacitinib, upadacitinib

207
Q

JAK Inhibitors renal and hepatic dose changes?

A

Need dose changes for both.

Upadacitinib does not have dose changes in renal disease

208
Q

JAK inhibitors drug interactions

A

Baricitinib- OAT3 inhibitors (probenecid)
Strong CYP3A4 inhibitors or inducers
Do not use bDMARDs, live vaccines, azathioprine, or cyclosporine

209
Q

When to use corticosteroids in RA

A 
Bridging therapy (before DMARDs are effective)
Continuous low dose therapy
Bursts for acute flares
210
Q

Corticosteroids for RA dose

A

Normal: prednisone 5-30mg QD

Immunosuppressive dose- pred 2 mg/kg/day or >20 mg /day for >14 days

211
Q

AE of corticosteroids

A

Hypothalamic pituitary adrenal suppression, cushings disease, osteoporosis, myopathies, glaucoma, cataracts, gastritis, HTN, hirsutism, electrolyte changes, glucose intolerance, skin atrophy, infection risk

212
Q

Biosimilar

A

Biological product that is highly similar to the reference product.
Must be same dosage form, route of administration, and strength
Must be demonstrates as safe and effective as reference

213
Q

Pregnancy and RA tx

A

Shorter acting NSAIDs (NOT COX-2) in 1st and 2nd trimester
Prednisone at lowest effective dose
Hydroxychloroquine
Sulfasalazine- with folic acid supplement
Certolizumab

214
Q

Lactation and Ra tx

A

Entanercept, hydroxychloroquine, ibuprofen, prednisone, sulfasalazine (only full term)

215
Q

Migraine characteristics

A

Age of onset: 15-35 yo
Gender prevalence: 3:1 women to men
Common migraine: without aura
Classic migraine: with aura

216
Q

S/S of migraine

A

HA duration of 4-72 hours
Pain with two of the following: intense, pulsatile, unilateral, exacerbated by activity
Accompanied by one of the following: N/V, photo/phonophobia, osmophobia

217
Q

Migraine POUND

A 
Pulsatile
One day duration (4-72 h)
Unilateral
N/V
Disabling intensity
218
Q

Phases of migraine attack

A

Prodromal- hours to days prior to migraine. Triggers.
Aura- sensory, motor, or focal neurological changes. Lasts less than 1 hour.
HA- lasts 4-72 hours
Postdromal- lethargy, irritability

219
Q

Theories of migraine moa

A

Vascular theory- reduced cerebral blood flow followed by extracranial vasodilation
Neural- cortical-spreading depression. Brain stem could send pain signals to cortex
Integrated neurovascular theory- neurogenic inflammation and the trigeminal nerve

220
Q

Vasoconstriction of cranial vessels in migraine

A

Vasodilation may be a causative factor in migraines.

Ergots and sumatriptan are both vasoconstrictors.

221
Q

Pathophysiology of migraine

A

Central migraine “generator” in cortex or brainstem. Possible due to defect in calcium channels mediating 5-HT and/or glutamate.
Peripheral pain mechanisms in meninges are initiated leading to neurogenic inflammation.
Nociceptive afferents carry pain signals to cortex.

222
Q

Inhibition of neurogenic inflammation in migraines

A

The trigeminal nerve innervates the blood vessels on the dura and transmits pain signals. Stimulation of the trigeminal ganglion releases proinflammatory neuropeptides which produce vasodilation and activate pain signals.
Many drugs inhibit neurogenic inflammation

223
Q

Trigeminal system and migraine

A

5-HT1B- causes vasoconstriction
5HT1D- inhibits substance P
5HT1F- Involved with pain signals

224
Q

Neurogenic inflammation involves

A

Brainstem trigger
Trigeminal activation
Release of vasoactive peptides
Vascular distention/inflammation/protein extravasation
Pain impulses via trigeminal nerve to trigeminal nucleus to cortex

225
Q

Drugs to treat migraines

A

APAP, NSAIDs, dopamine antagonists, opioids, serotonergic agents

226
Q

Symptomatic relief for mild to moderate migraine

A

APAP + caffeine
Metoclopramide
Midrin

227
Q

Abortive-type therapy: migraine specific drugs

A

Ergots

Triptans

228
Q

Is tolerability an issue with triptans?

A

No

229
Q

What is the only selective 5HT1F agonist?

A

Lasmiditan

230
Q

Prophylactic tx for migraines

A

Tricyclic antidepressants, beta blockers, anti-epileptics, CCBs, serotonin antagonists, botox

231
Q

MIDAS

A

Migraine disability assessment test

232
Q

Acute antimigraine agents

A

Nonspecific- OTC analgesics, NSAIDs, sympathomimetic agents, antiemetics
Specific agents- triptans, ergot alkaloids, ditans, gepants

233
Q

What meds are not recommended for migraines

A

Opioids

Butalbital containing agents

234
Q

Stratification according to severity of migraine

A

Mild
Moderate-severe
Extremely severe

235
Q

Mild migraine analgesic approach

A

NSAIDs
Excedrin (APAP, ASA, Caffeine)
Isometheptene compounds
Metoclopramide to reduce N

236
Q

Moderate-severe analgesic approach migraines

A 
Triptan tailored to individual needs +/- NSAID
Ditan
Gepants
Ergotamine derivatives 
Metoclopramide to reduce N
237
Q

Extremely severe analgesic approach migraines

A 
DHE IV or SQ sumatriptan
Ketorolac
Dexamethasone
Magnesium sulfate
Other additions- metoclopramide, dopamine antagonists, opioids
ER visit
238
Q

Prostaglandin inhibitors in migraine

A

Effective in mild-moderate migraine.
Reduce the neurogenic inflammation in trigeminal vascular system.
Ibuprofen, naproxen, Excedrin Migraine

239
Q

Sympathomimetics/combinations in migraines

A

APAP/ASA/Caffeine
Isometheptane/dichloralphenazone/APAP
Psuedophedrine

240
Q

Non selective acute migraine 5HT1 agonists

A

ergotamine

Dihydroergotamine

241
Q

Group I Triptans

A

Sumatriptan, Zolmitriptan, Rizatriptan, Almotriptan, Eletriptan
Faster onset, higher potency, higher recurrence

242
Q

Group II Triptans

A

Naratriptan, Frovatriptan

Slower onset, lower potency, lower recurrence

243
Q

Which triptans have the longest Tmax?

A

Naratriptan and frovatriptan (2-3 hours)

244
Q

Longer 1/2 life of triptans=

A

Less recurrence

245
Q

Which triptans have the longest 1/2 lifes?

A

Naratriptan, Frovatriptan
Eletriptan is in the middle
Lowest recurrence

246
Q

Which triptan has the poorest oral bioavailabilty?

A

Sumatriptan

247
Q

What triptan has the nest oral bioavailability?

A

Naratriptan, Almotriptan

248
Q

Triptans with non oral preparations

A

Sumatriptan- nasal spray, SQ, supp

Zolmitriptan- nasal spray

249
Q

Which triptans have the longest OOA

A

Naratriptan and Frovatriptan

250
Q

Which triptans have the fastest OOA?

A

Sumatriptan injection and spray

Oral triptans are around 30 min

251
Q

Contraindications of eletriptan

A

Contraindicated within 72 hours of potent 3A4 inhibitor (erythromycin, azoles)

252
Q

DDI of naratriptan

A

Oral contraceptives- decrease cl of N

Cigarettes- Increase cl of N

253
Q

DDI of Rizatriptan

A

Propranolol increases AUC of R

254
Q

DDI of Zolmitriptan

A

Propranolol, oral contraceptives, cimetidine- increase AUC of Z
Z increases AUC of APAP

255
Q

Which triptan has no DDI?

A

Frovatriptan

256
Q

Advantages of zolmitriptan

A

Melt for N or convenience

257
Q

Triptan symptoms

A 
Tingling sensation involving the head or any other part of the body
Numbness
Strange feeling
Sensation of warmth, heat, burning, cold
Pressure sensations
Anxiety
Agitation
258
Q

Safety of triptans

A

RIsk of CV events low, but do not use in severe Cv disease

259
Q

Contraindications of triptan therapy

A 
Uncontrolled HTN
Ischemic disease
Prinz-Metal angina
Cardiac arrhythmias
Multiple risk factors for atherosclerotic vascular disease
Primary vasculopathies
Basilar and hemiplegic migraine
260
Q

What do you modify triptan therapy for?

A 
Recurrence
Partial response
Nonresponse
Inconsistency
Tachyphylaxis
261
Q

Recurrence

A

Occurs with all triptans
The overall average recurrence rate is 30%
2nd dose of same triptan useful for treating recurrence in most patients.
Naratriptan and frovatriptan have least recurrence
Triptan + COX2 or NSAID may also reduce recurrence rate

262
Q

What to do if you have a partial response to triptan?

A

Second dose of same triptan

263
Q

what to do if you have nonresponse to triptan

A

Try another triptan

264
Q

Which triptan has the worst inconsistency?

A

Sumatriptan due to poor bioavailability

265
Q

Which triptans have the best consistency rates?

A

Zolmitriptan, rizatriptan, eletriptan

266
Q

What to do if you have tachyphylaxis on triptan

A

(falling off response after repeated use)

Switch to a diff triptan

267
Q

Dihydroergotamine (DHE) for migraines

A

Efficacy compared to triptans
Not orally available- IV, IM/SQ/ Nasal
Do not use in CV issues
Pregnancy category X

268
Q

Lasmiditan

A

5-HT1F agonist
Little or no CV issues
Recommended not to drive for 8 hours
Scheduled V controlled

269
Q

Ubrogepant

A

Acute migraine w or w/o aura

Contraindicated with potent 3A4 inhibitor

270
Q

Rimegepant

A

Acute migraine w or w/o aura
ODT, do not repeat w/in 24 hours
Avoid with strong inhibitors or inducers of 3A4

271
Q

When are the use of gepants, ditans, or neuromodulatory devices appropriate?

A

Licensed clinician
>18 yo
ICHD-3 migraine diagnosis
Either of the following:
Contraindication or inability to tolerate triptan
Inadequate response to two or more oral triptans

272
Q

Prophylactic antimigraine agents

A

Antiepileptic drucs, Beta blockers, CGRP i, antidepressants, gepant, triptan, NSAID

273
Q

Goals of preventative therapy

A

Reduce attack frequency, severity, duration, disability

274
Q

Indications for prophylaxis (migraines)

A

Attacks significantly interfere with pts daily routines
Frequent attacks
Contraindication to , failure, or overuse of acute tx (>10/month tx)
AE
Patient preference

275
Q

Migraine prophylaxis success

A

50% reduction in frequency of days w/ HA or migraine
Significant decrease in attack duration and severity
Improved response to acute tx
Reduction in migraine related disability
QOL increased
Allow 2 months to take effect

276
Q

Migraine prophylaxis anticonvulsants

A

Divalproex

  • use especially for pts with bipolar or seizures
  • Topiramate
277
Q

Migraine prophylaxis beta blockers

A

Metoprolol, timolol, propranolol

Takes 1-2 weeks to see effect

278
Q

Migraine prophylaxis antidepressants

A

No Level A recommendation

Amitriptyline, venlafaxine

279
Q

Migraine prophylaxis NSAIDs

A

Fenoprofen, Ibu, ketorolac, naproxen, celecoxib

280
Q

CGRP inhibitors

A

New migraine tx
expensive
erenumab, fremanezum, galcanezumab, eptinezumab

281
Q

Indications for treatment with monoclonal antibodies to CGRP

A

Licensed medical provider
>18 yo
Specific criteria based on HA, lack of response to other tx, functional assessments

282
Q

Natural/herbal for migraine prevention

A

Butterbur extract (Petasites hybridus 75 mg BID)

283
Q

Prophylaxis of mestrual migraines

A

NSAID 3-5 days prior and throughout menstruation

Naproxen 550mg BID

284
Q

Characteristics of lupus

A

Female, aged 15-45
More common in non-caucasians
All cause mortality rates 2.6 fold
First degree relatives with FH of SLE have 6 fold higher risk of developing SLE and 4 times higher risk of developing other autoimmune disease

285
Q

Current treatment landscape of lupus nephritis

A

Induction treatment- glucocoticoids + NIH IV, Euro-lupus IV, mycophenolate
Maintenance treatment- Mycohenolate, Azathioprine

286
Q

Mycophenolate (MMF) MOA

A

Inactive prodrug that is hydrolyzed to active MPA. MPA inhibits lymphocyte proliferation and lymphocyte migration; anti-fibrotic activity

287
Q

Mycophenolate AE

A

GI (D most common), leukopenia, anemia, hepatotoxicity, infections; lymphoproliferative malignancies
Caution in pregnancy and lactation

288
Q

Mycophenolate follow up

A

CBC, LFTs weekly with dose changes and then CBC every 1-3 months

289
Q

Myfortic

A

Some patients will tolerate Myfortic when they have experienced severe GI AE from MMF

290
Q

Cyclophosphamide (CYC)

A

Inactive prodrug that is activated by hepatic cyp450 enzymes.
Causes bone marrow suppression and infection, hemorrhagic cystitis, bladder cancer
Caution in pregnancy and lactation

Therapeutics 4 (8 decks)

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