Exam 4 Flashcards

1
Q

What parts of the GI tract are affected by ulcerative colitis?

A

rectum and colon

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2
Q

Does smoking have a protective effect in ulcerative colitis or Crohn’s disease?

A

ulcerative colitis

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3
Q

What drug classes may trigger disease flares in IBD?

A

NSAIDs and antibiotics

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4
Q

What drug class should generally be avoided in patients with IBD?

A

NSAIDs

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5
Q

Is enteral or parenteral nutrition used as nonpharmacologic therapy for IBD?

A

enteral nutrition

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6
Q

What are ADRs of sulfasalazine?

A

-N/V
-HA
-anorexia
-rash
-anemia
-hepatotoxicity
-thrombocytopenia
-hypersensitivity reactions (sulfonamide allergy)

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7
Q

What are monitoring parameters for sulfasalazine?

A

-CBC and LFTs at baseline, QOW for 3 months, QM for 3 months, then periodically
-BUN/SCr periodically

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8
Q

What are drug interactions with sulfasalazine?

A

-antiplatelets
-anticoagulants
-NSAIDs

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9
Q

Do sulfasalazines or mesalamines have more ADRs?

A

sulfasalazines

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10
Q

What are the formulations of mesalamine?

A

-topical (enema)
-suppository
-oral

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11
Q

For what type of ulcerative colitis are topical formulations of mesalamine used for?

A

left-sided disease

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12
Q

For what type of ulcerative colitis are suppository formulations of mesalamine used for?

A

proctitis

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13
Q

What is the specific dosage form of oral formulations of mesalamine?

A

delayed/controlled release

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14
Q

What are ADRs of mesalamine?

A

-N/V
-HA

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15
Q

What are drug interactions with mesalamine?

A

-antiplatelets
-anticoagulants
-NSAIDs
-agents affecting gastric pH

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16
Q

What is the indication of corticosteroids for use in IBD?

A

induction of remission

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17
Q

What are ADRs of systemic corticosteroids?

A

-hypocalcemia
-hypovitaminosis D

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18
Q

What are monitoring parameters for systemic corticosteroids?

A

occasional bone mineral density scans

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19
Q

What patients taking corticosteroids for IBD should be receiving occasional bone mineral density scans?

A

->60 y/o
-risk of osteoporosis
-using steroids for >3 months
-recurrent steroid user

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20
Q

What is a benefit of budesonide based on its mechanism of action?

A

minimal systemic exposure due to extensive first pass metabolism

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21
Q

Is azathioprine or mercaptopurine a prodrug?

A

azathioprine

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22
Q

What are the indications of azathioprine and mercaptopurine for use in IBD?

A

-fail ASA and/or refractory to/dependent on steroids
-maintenance of remission

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23
Q

What are ADRs of azathioprine and mercaptopurine?

A

-N/V
-diarrhea
-anorexia
-stomatitis
-bone marrow suppression
-hepatotoxicity
-fever
-rash
-arthralgia
-pancreatitis

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24
Q

What are the monitoring parameters for azathioprine and mercaptopurine?

A

-TPMT at baseline
-CBC and LFTs at baseline, QW for 1 month, Q1-2W after dose change, Q1-3M

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25
Q

What are the indications of cyclosporine for use in IBD?

A

-induction of remission for refractory UC
-refractory to/dependent on steroids

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26
Q

What are ADRs of cyclosporine?

A

-nephrotoxicity
-neurotoxicity
-HTN
-HLD
-hyperglycemia
-GI upset
-gingival hyperplasia
-hirutism

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27
Q

What are the monitoring parameters for cyclosporine?

A

-BP at baseline, every visit
-BUN/SCr at baseline, Q2W until stable, periodically
-LFTs at baseline, Q2W until stable, periodically
-cyanuric acid trough concentration baseline

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28
Q

What type of substrate is cyclosporine?

A

CYP3A and P-glycoprotein substrate

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29
Q

What is the indication of methotrexate for use in IBD?

A

induction of remission for CD

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30
Q

What are ADRs of methotrexate?

A

-bone marrow suppression
-N/V
-diarrhea
-stomatitis
-mucositis
-cirrhosis
-hepatitis
-fibrosis
-hypersensitivity pneumonitis
-rash
-urticaria
-alopecia

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31
Q

What are monitoring parameters for methotrexate?

A

-chest X-ray at baseline
-CBC, SCr, LFTs at baseline, Q4-8W

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32
Q

What are contraindications for methotrexate?

A

-pregnancy
-pleural effusions
-chronic liver disease/alcohol abuse
-immunodeficiency
-preexisting blood dyscrasias
-leukopenia/thrombocytopenia
-CrCl < 40 mL/min

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33
Q

What are the TNF-α inhibitor ADRs?

A

-increased risk of serious infections
-injection site reactions (SQ) and infusion related reactions (IV)
-risk of malignancy
-hepatosplenic T-cell lymphoma (HSTCL) risk
-risk of demyelinating disease
-may exacerbate CHF
-development of anti-drug antibodies

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34
Q

When should TNF-α inhibitors be avoided?

A

active infection

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35
Q

What monitoring parameters in regards to infections should be measured before treatment initiation?

A

-PPD skin test for TB
-chest X-ray
-hepatitis B and C

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36
Q

What is a good recommendation for TNF-α inhibitors?

A

ensure vaccinations are up to date

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37
Q

What is contraindicated during TNF-α inhibitor therapy?

A

live vaccines during treatment and for three months after

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38
Q

What patients are contraindicated for TNF-α inhibitor therapy?

A

-cancer
-demyelinating CNS disease
-optic neuritis
-NYHA Class III/IV HF

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39
Q

What are baseline monitoring parameters for TNF-α inhibitors?

A

-chest X-ray
-PPD skin test for TB
-s/s of infection
-urinalysis
-CBC
-SCr
-electrolytes
-LFTs
-hepatitis B and C

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40
Q

What baseline monitoring parameters are different from the maintenance for TNF-α inhibitors?

A

-chest X-ray
-PPD skin test for TB
-hepatitis B and C

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41
Q

What maintenance monitoring parameter is different from the baseline for TNF-α inhibitors?

A

inflammatory markers

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42
Q

How often should monitoring occur for TNF-α inhibitors?

A

Q8-12W

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43
Q

What are the indications for infliximab?

A

-moderate to severe active CD and UC
-induction and maintenance therapy

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44
Q

What is the route of administration for infliximab?

A

IV

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45
Q

What drugs can be used concomitantly with infliximab for increased efficacy?

A

immunosuppressives

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46
Q

When is there an increased HSTCL risk for infliximab?

A

co-administeration with azathioprine

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47
Q

What are monitoring parameters specific to infliximab?

A

-vitals
-infusion reactions

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48
Q

What are the indications for adalimumab?

A

-moderate to severe active CD and UC
-induction and maintenance therapy

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49
Q

What is the route of administration for adalimumab?

A

SQ

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50
Q

What are the indications for golimumab?

A

-moderate to severe active UC
-induction and maintenance therapy

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51
Q

What is the route of administration for golimumab?

A

SQ

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52
Q

What are the indications for certolizumab pegol?

A

-moderate to severe active CD
-induction and maintenance therapy

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53
Q

What is the route of administration for golimumab?

A

SQ

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54
Q

What TNF-α inhibitor has the highest risk of developing ADAs?

A

infliximab

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55
Q

What are the TNF-α inhibitor drugs?

A

-infliximab
-adalimumab
-certolizumab pegol
-golimumab

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56
Q

What is the mechanism of action of natalizumab?

A

anti-α subunit of integrins

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57
Q

What are the indications for natalizumab?

A

-CD
-induction and maintenance of therapy

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58
Q

What drugs can natalizumab not be used with?

A

-immunosuppressants
-TNF-α inhibitors

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59
Q

What is the route of administration for natalizumab?

A

IV

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60
Q

When should natalizumab be discontinued in patients?

A

-no benefit by 12 weeks (3 cycles) and/or
-steroid-dependent within 6 months

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61
Q

What is an ADR associated with natalizumab?

A

PML

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62
Q

What causes an increased risk of PML with natalizumab use?

A

-longer duration of therapy (> 2 years)
-prior immunosuppressant use
-JC antibody positive

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63
Q

What is the mechanism of action of vedolizumab?

A

anti-α4β77 integrin antibody

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64
Q

What are the indications for vedolizumab?

A

-CD and UC
-induction and maintenance therapy

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65
Q

What is the route of administration for vedolizumab?

A

IV

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66
Q

What is the mechanism of action of ustekinumab?

A

IL-12 and IL-23 antagonist

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67
Q

What are the indications for ustekinumab?

A

-CD and UC
-induction and maintenance therapy

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68
Q

What is the route of administration for ustekinumab?

A

SQ

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69
Q

What is the mechanism of action of risankizumab-rzaa?

A

selective IL-23 antagonist

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70
Q

What are the indications for risankizumab-rzaa?

A

-moderate to severe active CD and UC
-induction and maintenance therapy

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71
Q

What are the routes of administration for risankizumab-rzaa?

A

IV and SQ

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72
Q

What are common ADRs of risankizumab-rzaa?

A

-headache
-nasopharyngitis
-arthralgia
-abdominal pain
-anemia
-nausea

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73
Q

What are ADRs associated with risankizumab-rzaa?

A

-potential hepatotoxicity
-increase in lipids

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74
Q

What are baseline monitoring parameters for risankizumab-rzaa and mirikizumab-mrkz?

A

-chest X-ray
-PPD skin test for TB
-hepatitis B and C
-lipids
-LFTs
-renal function
-s/s of infection

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75
Q

What is the mechanism of action of mirikizumab-mrkz?

A

IL-23p19 antagonist

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76
Q

What are the indications for mirikizumab-mrkz?

A

-moderate to severe active UC
-induction and maintenance therapy

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77
Q

What are the routes of administration for mirikizumab-mrkz?

A

IV and SQ

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78
Q

What are common ADRs of mirikizumab-mrkz?

A

-headache
-arthralgia
-rash
-injection site reaction

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79
Q

What is an ADR associated with mirikizumab-mrkz?

A

potential hepatotoxicity

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80
Q

What criteria need to be confirmed to determine that an IBD patient is at treatment failure?

A

-inflammation
-exclude infection and noncompliance to treatment
-serum drug therapeutic and ADA levels

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81
Q

What type of treatment failure is a combination of subtherapeutic drug levels and detectable ADAs?

A

immune mediated pharmacokinetic failure

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82
Q

What is the next step of therapy for immune mediated pharmacokinetic failure?

A

change to alternate drug within the same class +/- immunomodulator

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83
Q

What type of treatment failure is a combination of subtherapeutic drug levels and undetectable ADAs?

A

non-immune mediated pharmacokinetic failure

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84
Q

What is the next step of therapy for non-immune mediated pharmacokinetic failure?

A

increase dose

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85
Q

What type of treatment failure is a combination of therapeutic drug levels and detectable ADAs?

A

false positive or mechanistic failure

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86
Q

What is the next step of therapy for a false positive?

A

repeat TDM levels

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87
Q

What type of treatment failure is a combination of therapeutic drug levels and undetectable ADAs?

A

mechanistic failure

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88
Q

What is the next step of therapy for mechanistic failure?

A

switch to different biologic class agent

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89
Q

What are the other biologic drugs?

A

-natalizumab
-vedolizumab
-ustekinumab
-risankizumab-rzaa
-mirikizumab-mrkz

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90
Q

What is the mechanism of action of tofacitinib?

A

JAK inhibitor

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91
Q

What is the route of administration for tofacitinib?

A

oral

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92
Q

What is the indication for tofacitinib?

A

UC

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93
Q

What are the clinical pearls for tofacitinib and upadacitinib?

A

-rapid onset
-should NOT be used with immunosuppressants or biologics
-short half-life
-eliminated via hepatic metabolism and renal excretion

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94
Q

How much should the dose of tofacitinib be decreased by for moderate/severe renal impairment or moderate hepatic impairment?

A

50%

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95
Q

When should tofacitinib be avoided?

A

-severe hepatic impairment
-strong CYP3A inducer

96
Q

What are the drug interactions for tofacitinib?

A

-moderate or strong CYP3A inhibitor with strong CYP2C19 inhibitor
-strong CYP3A inducer

97
Q

How much should the dose of tofacitinib be decreased by for use of moderate or strong CYP3A inhibitors with a strong CYP2C19 inhibitor?

A

50%

98
Q

What are common ADRs of tofacitinib?

A

-diarrhea
-elevated cholesterol
-headache
-shingles
-increased creatine phosphokinase
-nasopharyngitis
-rash
-URI

99
Q

What are rare ADRs of tofacitinib?

A

-malignancy
-serious infection
-neutropenia
-hypersensitivity

100
Q

What is the black box warning for tofacitinib and upadacitinib?

A

-increased mortality in RA pts ≥ 50 y/o with at least one CV risk factor
-thrombosis

101
Q

What are baseline monitoring parameters for tofacitinib?

A

-chest X-ray
-PPD skin test for TB
-hepatitis B and C
-ANC
-CBC
-lipids
-LFTs
-infection
-skin exam

102
Q

What is the mechanism of action of upadacitinib?

A

selective JAK1 inhibitor

103
Q

What is the route of administration for upadacitinib?

A

oral

104
Q

What are the indications for upadacitinib?

A

CD and UC

105
Q

When are dose adjustments for upadacitinib required?

A

-renal impairment
-mild to moderate hepatic impairment

106
Q

When is upadacitinib not recommended?

A

-ESRD
-severe hepatic impairment
-strong CYP3A inducer

107
Q

What are the drug interactions for upadacitinib?

A

-strong CYP3A inhibitor
-strong CYP3A inducer

108
Q

What are common ADRs of upadacitinib?

A

-URI
-acne
-increased creatine phosphokinase
-elevated cholesterol
-headache
-shingles

109
Q

What are rare ADRs of upadacitinib?

A

-malignancy
-serious infection
-increase in LFTs
-anemia
-neutropenia
-lymphopenia
-hypersensitivity
-tetratogenicity

110
Q

What is another baseline monitoring parameter for upadacitinib in addition to tofacitinib?

A

ALC

111
Q

What is the mechanism of action of ozanimod?

A

selective sphingosine-1-phosphate (S1P) receptor modulator

112
Q

What is the route of administration for ozanimod?

A

oral

113
Q

What is the indication for ozanimod?

A

moderate to severe active UC

114
Q

What are the contraindications for ozanimod?

A

-patients experiencing the following in the last six months: MI, unstable angina, stroke, TIA, decompensated HF requiring hospitalization, class III/IV HF
-Mobitz type II 2nd or 3rd degree AV block, sick sinus syndrome, or SA block unless patient has functioning pacemaker
-severe untreated sleep apnea
-MAO inhibitor

115
Q

What is ozanimod metabolized by?

A

-ALDH/ADH
-CYP3A4

116
Q

What are the ADRs of ozanimod and estrasimod?

A

-increased risk of infection
-bradycardia/AV conduction delays
-liver injury/elevated transaminases
-moderate increase in SBP
-respiratory effects
-macular edema
-reversible posterior leukoencephalopathy syndrome (RPLS)/posterior reversible encephalopathy syndrome (PRES)

117
Q

What are the drug interactions with ozanimod?

A

-adrenergic and serotonergic drugs
-combination BB and CCB
-foods high in tyramine
-MAO inhibitors
-strong CYP2C8 inhibitors
-strong CYP2C8 inducers

118
Q

What are the baseline monitoring parameters for ozanimod and estrasimod?

A

-chest X-ray
-PPD skin test for TB
-hepatitis B and C
-CBC
-LFTs
-infection
-BP
-spirometry
-ECG
-eye exam

119
Q

What monitoring parameters for ozanimod and estrasimod are only measured at baseline?

A

-chest X-ray
-PPD skin test for TB
-hepatitis B and C
-ECG

120
Q

What is the mechanism of action of estrasimod?

A

selective sphingosine-1-phosphate (S1P) receptor modulator

121
Q

What is the route of administration for estrasimod?

A

oral

122
Q

What is the indication for estrasimod?

A

moderate to severe active UC

123
Q

What are the contraindications for estrasimod?

A

-patients experiencing the following in the last six months: MI, unstable angina, stroke, TIA, decompensated HF requiring hospitalization, class III/IV HF
-various cardiac conduction abnormalities

124
Q

What is estrasimod metabolized by?

A

-CYP2C8
-CYP2C9
-CYP3A4

125
Q

What are the new small molecule drugs?

A

-tofacitinib
-upadacitinib
-ozanimod
-estrasimod

126
Q

What are the antimicrobial drugs?

A

-ciprofloxacin
-metronidazole
-rifamycin antibiotics

127
Q

What is the indication of antimicrobials for use in IBD?

A

adjunctive therapy for treatment of complications

128
Q

What are the ADRs of antimicrobials?

A

-agent-specific ADRs
-resistance
-C. diff

129
Q

What objective markers are only affected by acute liver injury?

A

-AST
-ALT
-alkaline phosphatase

130
Q

How is AST affected by acute liver injury?

A

increased

131
Q

How is ALT affected by acute liver injury?

A

increased

132
Q

How is alkaline phosphatase affected by acute liver injury?

A

increased

133
Q

How is bilirubin affected by acute liver injury and chronic liver disease?

A

increased

134
Q

How is albumin affected by chronic liver disease?

A

decreased

135
Q

How is INR affected by chronic liver disease?

A

increased

136
Q

How is thrombocytopenia affected by chronic liver disease?

A

decreased

137
Q

What are the classifications of drug-induced liver injury?

A

-direct hepatotoxicity
-idiosyncratic hepatotoxicity
-indirect hepatotoxicity

138
Q

What are high-risk medications for drug-induced liver injury?

A

-acetaminophen
-anti-infectives

139
Q

What dose of acetaminophen is considered a high dose?

A

≥ 8 g

140
Q

What are the signs and symptoms of acetaminophen overdose?

A

-abdominal pain
-jaundice
-N/V
-diarrhea

141
Q

When should activated charcoal be administered for acetaminophen overdose?

A

within 1-2 hours of ingestion

142
Q

When should NAC be administered for acetaminophen overdose?

A

≥ 4 hours after ingestion

143
Q

For the Rumack-Matthew Nomogram, which side of the line indicates treatment with NAC?

A

right

144
Q

What formulation of NAC is preferred for acetaminophen overdose?

A

oral

145
Q

What are the monitoring parameters for NAC?

A

-liver enzymes Q12-24H
-s/s of acute liver injury

146
Q

What class of drugs should be avoided with cirrhosis?

A

NSAIDs

147
Q

What are causative factors of cirrhosis?

A

-chronic alcohol use
-viral hepatitis
-metabolic liver disease
-cholestatic liver disease
-drugs

148
Q

What are the signs and symptoms of cirrhosis?

A

-pruritus
-fatigue
-weight loss
-ascites
-jaundice
-hepatomegaly or splenomegaly
-encephalopathy

149
Q

What are the assessment tools for severity of cirrhosis?

A

-Child-Pugh
-Model for End Stage Liver Disease (MELD)

150
Q

What are the signs and symptoms of ascites?

A

-abdominal distention
-abdominal pain
-SOB
-nausea

151
Q

What are nonpharmacological treatments for management of ascites?

A

-sodium restriction (< 2 g/day)
-assessment for liver transplant

152
Q

What is the first-line treatment for ascites?

A

spironolactone and furosemide

153
Q

What is the second-line treatment for ascites?

A

-paracentesis
-TIPS

154
Q

What is the initial dose of spironolactone/furosemide?

A

100 mg/40 mg

155
Q

How often should spironolactone/furosemide be titrated?

A

every 3-5 days

156
Q

What is the maximum dose of spironolactone/furosmide?

A

400 mg/160 mg

157
Q

Is spironolactone or furosemide preferred if choosing monotherapy?

A

spironolactone

158
Q

What are side effects of spironolactone?

A

-AKI
-hyperkalemia
-gynecomastia

159
Q

What are side effects of furosemide?

A

-AKI
-hypokalemia

160
Q

What are the monitoring parameters of diuretics for the treatment of ascites?

A

-s/s of ascites
-SCr
-potassium

161
Q

When should albumin be administered in the case of paracentesis?

A

> 5 L removed

162
Q

What is the dose of albumin for ascites?

A

25% albumin IV

163
Q

What is the dosing of albumin for ascites?

A

6-8 g of albumin/liter removed

164
Q

What are the risk factors for esophageal varices?

A

-varices size
-cirrhosis severity
-red color markings on endoscopy
-active alcohol use

165
Q

What are the treatment options for variceal bleeding prophylaxis?

A

-NSBB
-EVL

166
Q

Which NSBBs are used for esophageal varices?

A

-nadolol
-propranolol
-carvedilol

167
Q

How often should NSBBs be titrated for esophageal varices?

A

every 3 days until goal achieved

168
Q

What are the side effects of NSBBs?

A

-drowsiness or insomnia
-bradycardia
-hypotension

169
Q

What is the target HR when taking NSBBs?

A

55 to 60 bpm

170
Q

What is the target SBP when taking NSBBs?

A

> 90 mm Hg

171
Q

What drugs should not be used to treat esophageal varices?

A

-PPIs
-vitamin K

172
Q

What is the initial treatment for variceal bleeding acute management?

A

-blood transfusion
-octreotide
-antibiotic prophylaxis

173
Q

What type of drug is octreotide?

A

vasoconstrictor

174
Q

How long should octreotide be used for?

A

2 to 5 days

175
Q

What are the side effects of octreotide?

A

-N/V
-HTN
-bradycardia
-hyperglycemia

176
Q

What are the monitoring parameters of octreotide?

A

-s/s of N/V
-BP
-HR
-BG

177
Q

What antibiotics should be used in liver disease?

A

third generation cephalosporins

178
Q

What is a side effect of third generation cephalosporins?

A

diarrhea

179
Q

What is a monitoring parameter of third generation cephalosporins?

A

s/s of infection

180
Q

What is the maximum duration of use for antibiotic prophylaxis?

A

7 days

181
Q

When should an EVL be performed?

A

within 12 hours of presentation

182
Q

What are the treatments for secondary prophylaxis of variceal bleeding?

A

-EVL every 1 to 4 weeks
-NSBBs indefinitely until decompensation

183
Q

What are the signs and symptoms of hepatic encephalopathy?

A

-jaundice
-delirium
-convulsions
-coma

184
Q

What are the objective markers of hepatic encephalopathy?

A

-EEG
-evoked potentials

185
Q

What is the first-line treatment for hepatic encephalopathy?

A

lactulose 25 mL BID

186
Q

What is the diagnostic level of polymorphonuclear (PMN) leukocytes for spontaneous bacterial peritonitis?

A

≥ 250 cells/mm^3

187
Q

What is the duration of use of third generation cephalosporins for treatment of spontaneous bacterial peritonitis?

A

5 to 7 days

188
Q

What is the dosing of albumin for day 1 of spontaneous bacterial peritonitis?

A

1.5 g/kg for one dose

189
Q

What is the dosing of albumin for day 3 of spontaneous bacterial peritonitis?

A

1 g/kg for one dose

190
Q

How soon should albumin be administered after diagnosis of spontaneous bacterial peritonitis?

A

within 6 hours

191
Q

What drugs are used for secondary prophylaxis of spontaneous bacterial peritonitis?

A

-sulfamethoxazole/trimethoprim
-ciprofloxacin

192
Q

What are the monitoring parameters for sulfamethoxazole/trimethoprim?

A

-SCr
-electrolytes
-CBC

193
Q

What are the monitoring parameters for ciprofloxacin?

A

-mental status
-CBC
-renal function

194
Q

How long should secondary prophylaxis be used for spontaneous bacterial peritonitis?

A

indefinitely

195
Q

What is the dosing frequency of secondary prophylaxis for spontaneous bacterial peritonitis?

A

QD

196
Q

What are the two types of stroke?

A

-ischemic
-hemorrhagic

197
Q

What are the two types of ischemic stroke?

A

-atherosclerotic
-cardioembolic

198
Q

What are the modifiable risk factors for stroke?

A

-CVD
-diabetes
-HLD
-HTN
-illicit drug/alcohol abuse
-obesity/physical inactivity
-cigarette smoking

199
Q

What is the clinical presentation of stroke?

A

-dysphagia
-facial droop
-unilateral or bilateral weakness
-ataxia
-vision changes
-headache

200
Q

What are the imaging diagnostic criteria for stroke?

A

-head CT
-MRI

201
Q

What are the vital signs diagnostic criteria for stroke?

A

-BP
-oxygen saturation

202
Q

What are the labs diagnostic criteria for stroke?

A

-BG
-BMP
-CBC
-INR
-aPTT

203
Q

What is the test diagnostic criteria for stroke?

A

-ECG

204
Q

When should hyperglycemia in a patient experiencing stroke be treated with an insulin drip?

A

acidosis

205
Q

How often should BP be checked in patients experiencing stroke?

A

-Q15 minutes for 2 hours
-Q30 minutes for 6 hours
-Q1H for 16 hours

206
Q

What is the BP goal for the first 48 hours for a patient experiencing ischemic stroke with no tPA administration?

A

< 220/110 mm Hg

207
Q

What is the BP goal for the first 48 hours for a patient experiencing ischemic stroke with tPA administration?

A

< 180/105 mm Hg

208
Q

When should the BP goal be lowered to the outpatient goal in a patient experiencing stroke?

A

after 48 hours

209
Q

What type of agents should treat hypertension in a patient experiencing stroke for the first 48 hours of admission?

A

parenteral

210
Q

What is the maximum dose of alteplase in stroke patients?

A

90 mg

211
Q

What is the maximum dose of tenecteplase in stroke patients?

A

25 mg

212
Q

Is alteplase or tenecteplase administered as an infusion?

A

alteplase

213
Q

When should antiplatelets and anticoagulants be avoided?

A

24 hours after administration of thrombolytics

214
Q

What type of stroke should thrombolytics be used for?

A

ischemic

215
Q

What are the inclusion criteria for use of thrombolytics in ischemic stroke patients?

A

-ischemic stroke
-symptom onset ≤ 4.5 hours
-age ≥ 18 y/o

216
Q

What is the first-line treatment for acute management of ischemic stroke?

A

aspirin

217
Q

How long should high-dose aspirin be administered for ischemic stroke patients?

A

2 to 4 weeks

218
Q

What are the monitoring parameters for antiplatelets?

A

-s/s of bleeding
-stroke

219
Q

When should aspirin and clopidogrel be used for ischemic stroke?

A

minor strokes (NIHSS ≤ 4)

220
Q

When should ticagrelor and aspirin be used for ischemic stroke?

A

minor strokes (NIHSS ≤ 5)

221
Q

What antiplatelets require loading doses?

A

-aspirin
-ticagrelor

222
Q

What is the protocol for an admitted stroke patient on an anticoagulant?

A

D/C and start aspirin

223
Q

When should an anticoagulant be initiated for stroke patients?

A

≥ 2 to 14 days after stroke

224
Q

What is the antidote for warfarin?

A

IV vitamin K

225
Q

What is the antidote for heparin products?

A

protamine

226
Q

What is the antidote for dabigatran?

A

idarucizumab

227
Q

What is the antidote for other DOACs?

A

recombinant coagulation factor Xa

228
Q

What is the BP goal for the first 24 hours for a patient experiencing hemorrhagic stroke?

A

< 180/110 mm Hg

229
Q

What is the BP goal after 24 hours for a patient experiencing hemorrhagic stroke?

A

< 160/90 mm Hg

230
Q

What is the BP goal after 48 hours for a patient experiencing hemorrhagic stroke?

A

< 140/90 mm Hg or < 130/80 mm Hg

231
Q

What type of stroke is prevention of vasospasm indicated for?

A

subarachnoid hemorrhagic stroke

232
Q

What is the treatment for prevention of vasospasm?

A

nimodipine 60 mg PO Q4H for 21 days after stroke

233
Q

Are anticonvulsants indicated for stroke patients?

A

no

234
Q

What are the first-line treatments for secondary stroke prevention antiplatelet therapy?

A

-aspirin
-dipyridamole/aspirin

235
Q

What is the second-line treatment for secondary stroke prevention antiplatelet therapy?

A

clopidogrel

236
Q

What is a first-line treatment for secondary stroke prevention antiplatelet therapy of minor stroke?

A

clopidogrel

237
Q

What is a second-line treatment for secondary stroke prevention antiplatelet therapy of moderate to severe stroke?

A

clopidogrel