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Rheumatology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Effects of Glucocorticosteroids

A

Anti-inflammatory
Bind & block promoter sites of proinflammatorty genes IL-1 alpha & IL-2 beta
Decreased production of TNF alpha
Multiple cell specific effects

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2
Q

Proinflammatory Mediators Glucocorticosteroids Inhibits

A 
Phospholipase A2
Cyclooxygenase 2
Nitric oxide synthetase
Prostaglandins
Leukotrienes
Thromboxanes
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3
Q

Effect of Glucocorticosteroids on Leukocytes

A

Can’t exit circulation as readily

Entry to site of infection & tissues injury impaired

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4
Q

Glucocorticosteroids & Suppression of Inflammatory Response

A

Increased neutrophils
Decreased eosinophils
Decreased monocytes
Decrease lymphocytes

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5
Q

Glucocorticosteroids & Effects of Acquired Immunity

A

Decreased APCs
Decreased T cells
Decreased B cells

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6
Q

Increased Infection Risk with Glucocorticosteroids

A

Immediate reduction of phagocytic responses

Main infections on long term therapy: herpes zoster, staph, candida

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7
Q

Monitoring for Toxicity of Glucocorticosteroids

A 
BP
Serum glucose
Lipid profile
Eye exam
Bone density
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8
Q

Pros of Steroids

A

No dose adjustment in renal impairment

Good symptom relief of pain secondary to inflammation

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9
Q

Short Term Symptom Management for RA

A

NSAIDs

Steroids

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10
Q

NSAIDs & RA

A

May alleviate the symptoms

Do not prevent irreversible joint damage

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11
Q

Glucocorticoids & RA

A

Quick symptoms relief
Avoid long term administration due to toxicities
Not a profound effect on decreasing joint destruction

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12
Q

DMARDs & RA

A

Variable response
Discontinuation rate high
Continued indefinitely unless significant toxicity
Biological & non-biological

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13
Q

Non-Biological DMARDs

A 
Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
D-penicillamine
Gold salt
Azithroprine
Cyclosporine
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14
Q

Biological DMARDs

A 
Etanercept (Enbrel)
Adilimumab (Humira)
Infliximab (Remicade)
Aakinra (Kineret)
Abatacept (Orencia)
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15
Q

2nd Line if Failure to Achieve RA Remission in 3 Months

A

Change DMARD

Go to combination therapy

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16
Q

How to decide on which drug for RA?

A

Disease severity
Prognostic factors
Patient preference

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17
Q

Methotrexate (Rheumatrex)

A

DMARD of choice for RA

Generally well tolerated

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18
Q

MOA of Methotrexate (Rheumatrex)

A

Stimulates adenosine release
Reduced neutrophil adhesion
Suppression of cell mediated immunity
Anti proliferative effect on synovial fibroblasts & endothelial
Inhibition of IL-1, IL-6, & IL-8
Inhibits synovial collegenase gene suppression

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19
Q

What do all patients on methotrexate need?

A

Folic acid supplemet

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20
Q

Contraindications of Methotrexate (Rheumatrex)

A

Women contemplating pregnancy
Pregnancy
Liver disease or excessive ETOH intake
GFR less than 30 mL/min

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21
Q

SE of Methotrexate (Rheumatrex)

A 
Hepatotoxicity
Pulmonary toxicity
Myelosuppression
Nephrotoxicity
Fatigue
Decreased ability to concentrate
Alopecia
Nausea
Stomach upset
Loos stools
Soreness of the mouth
Rash on the extremities
Headache
Fever
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22
Q

Toxicities of Methotrexate (Rheumatrex)

A

Myelosuppression
Hepatotoxicity including cirrhosis
Pulmonary toxicity

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23
Q

Monitoring of Methotrexate (Rheumatrex)

A 
CBC
LFTs
Albumin
Creatinine
Pre treatment CXR
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24
Q

2nd Line Drug for RA

A

Sulfasalazine (Azulfidine)

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25
Q

MOA of Sulfasalazine (Azulfidine)

A

Inhibition of PMN cell migration
Reduced lymphocyte responses
Inhibits angiogenesis
Decreases inflammatory cytokines & IgM RF production

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26
Q

Contraindications of Sulfasalazine (Azulfidine)

A 
Sulfa allergy
Pregnancy category D
GI or GU tract obstruction
Porphyria
Platelet count less than 50K
LFTs > 2x ULN
Hepatitis
Men wanting to conceive
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27
Q

SE of Sulfasalazine (Azulfidine)

A 
Nausea & diarrhea
Intestinal or urinary obstruction
Oral ulcers
Orange-yellow pigmentation of the skin
Headache
Depression
Neutropenia
Thrombocytopenia
Agranulocytosis
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28
Q

Toxicity of Sulfasalazine (Azulfidine)

A

Myelosuppression

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29
Q

Monitoring of Sulfasalazine (Azulfidine)

A

CBC monthly x3

CBC every 3 months

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30
Q

Effects Leflunomide (Avara)

A

Anti-inflammatory
Antiproliferative
Decreases progression of joint erosions & joint space narrowing

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31
Q

MOA of Leflunomide (Avara)

A

Competitive inhibitor of dihydrofolate reductase
Decreases production of pyrimidine
Inhibits pyrimidine synthesis

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32
Q

Contraindications to Leflunomide (Avara)

A

Pregnancy
Preexisting liver disease
Alcoholism

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33
Q

SE of Leflunomide (Avara)

A 
Diarrhea
Rash
Reversible alopecia
Hepatotoxicity
Weight loss
HTN
Bone marrow suppression
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34
Q

Leflunomide (Avara) Toxicities

A

Hepatotoxicity

Bone marrow suppression

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35
Q

Monitoring of Leflunomide (Avara)

A

Monthly x 6 then every 2 months
CBC
Liver enzymes
Creatinine

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36
Q

Interactions with Leflunomide (Avara)

A

Weak inhibitor of CYP2C9
Increase warfarin levels
Rifampin may increase levels of leflunomide
Bile acid sequesterants decrease effectiveness of leflunomide

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37
Q

Hydroxychloroquine (Plaquenil) & RA

A

Antimalarial

Does not limit progression of RA

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38
Q

Use of Hydroxychloroquine (Plaquenil)

A

Mild RA with no evidence of joint destruction & no inflammatory markers or autoimmune markers
Add-on to methotrexate

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39
Q

MOA of Hydroxychloroquine (Plaquenil)

A

Interferes with normal antigen processing
Inhibits lysosomal enzymes & IL-1 release
Inhibition of PMNs & lymphocyte responses

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40
Q

Toxicity of Hydroxychloroquine (Plaquenil)

A

Macular damage

41
Q

Monitoring with Hydroxychloroquine (Plaquenil)

A

Fundoscopic & visual field exams every 6-12 months

42
Q

SE of Hydroxychloroquine (Plaquenil)

A 
Nausea
Diarrhea
Abdominal discomfort
Photosnsitivity
Skin pigmentation changes
Rash
Macular damage
43
Q

Drug Interactions with Hydroxychloroquine (Plaquenil)

A

Decreased metabolism of beta blockers

May increase cyclosporine & digoxin levels

44
Q

Treatment of Severe RA

A

Combination of DMARD therapy
Switch to another TNF inhibitor with different mechanism
Ongoing glucocorticoid therapy
Ongoing NSAIDs

45
Q

TNF Inhibitors

A

Etanercept (Enbrel)
Infliximab (Remicade)
Adalimumab (Humira)

46
Q

MOA of TNF Inhibitors

A

Bind to TNF-alpha, cell lysis occurs

Interferes with inflammatory activity

47
Q

SE of TNF Inhibitors

A 
Injection site infections
Infusion reaction (infliximab-Remicade)
Serious infections leading to sepsis
Do not administer live vaccine
Response to other vaccines may be diminished
48
Q

Contraindications of TNF Inhibitors

A

Latent TB infection

High risk for opportunistic infections

49
Q

Interactions of Infliximab (Remicade)

A

Abatacept (Orencia)
Anakinra (Kineret)
Increased risk of infection

50
Q

Methotrexate & Infliximab (Remicade)

A

Decreases development of infliximab antibodies

51
Q

Toxicity of TNF Inhibitors

A

Injection site reaction

Increased risk of local or systemic infection

52
Q

Monitoring of TNF Inhibitors

A

PPD prior to therapy

Periodic CBC

53
Q

MOA of Anakinra (Kineret)

A

Blocks IL-1 receptor to decrease degree of joint destruction & inflammation

54
Q

Anakinra (Kineret) & GFR less than 30 mL/min

A

Decrease dose

55
Q

Contraindications of Anakinra (Kineret)

A

Sensitivity to E. coli-derived proteins
Preexisting infection or high risk for infection
Not to be used in combination with TNF inhibitors

56
Q

SE of Anakinra (Kineret)

A

Skin irruption at injection site
Infection
Possible angioedema & anaphylaxis
Decrease in WBCs

57
Q

Monitoring in Anakinra (kineret) Use

A

CBC monthly x3

CBC Q4 months x 1 year

58
Q

Non-preferred DMARDS

A

D-penicillamine
Azithroprine
Cyclosporine A
Gold compounds

59
Q

D-Penicillamine

A

Chelating agent for metal poisoning, arsenic poisoning, or Wilson’s disease
Depresses T cell activity
Pregnancy category D

60
Q

Aithroprine (Imuran)

A

Inhibits enzymatic activity required for DNA synthesis
Adjust dose for decreased renal clearance
Pregnancy category D
Major toxicity = bone marrow suppression
Carcinogenic

61
Q

Cyclosporine A

A

Blocks activation of T cells & IL-2
Follow blood levels
Many drug interactions
Toxicity: renal failure

62
Q

Gold Compounds

A

Decreases prostaglandin production
Add-on therapy
Greater toxicity than DMARDs

63
Q

Medications that May Lead to a SLE Exacerbation

A

Sulfa containing antibiotics
Minocycline
OCPs

64
Q

Medication that May Lead to Drug Induced Lupus

A

Procainamide
Hydralazine
Griseofulvin

65
Q

Medications that Work for Cutaneous & Musculoskeletal Involvement of SLE

A

Anti-malarials

Hydroxychloroqine (Plaquenil)

66
Q

Medications for Cutaneous Involvement of SLE

A

Topical therapies

67
Q

Medication for Musculoskeletal Involvement of SLE

A

NSAIDs

68
Q

Medications for Significant Organ Involvement in SLE

A

Glucocorticoids

69
Q

Immune Modulators for Severe SLE When Steroid Resistent

A 
Methotrexate
Cyclophosphamide
Azathiprine
Mycophenolate
Rituximab
70
Q

Medication When Antiphospholipid Antibody Positive in SLE

A

Warfarin

71
Q

Medications to Treat Acute Attacks of Gout

A

NSAIDs
Colchicine
Steroids

72
Q

Medications for Prevention of Gout

A 
Xanthine oxidase inhibitors: allopurinol (Zyloprim), febuxostat
Uricosuric drugs (Probenecid)
73
Q

MOA of NSAIDs

A

Inhibit cyclooxygenase & production of mediators of inflammation

74
Q

Contraindications of NSAIDs

A 
CrCl less than 60 mL/min
Active duodenal or gastric ulcers
HF
Uncontrolled HTN
Allergy
Chronic anticoagulation
75
Q

NSAIDs Increase Risk of

A 
CVA
MI
CHF
A-fib
CV death
76
Q

Aspirin & NSAIDs

A

Take aspirin 2 hours prior to NSAIDs

77
Q

NSAIDs Acute Gout

A

Indomethacin (Indocin)
Naproxen
Celecoxib (Celebrex)

78
Q

Colchicine for Acute Gout Attacks

A

NSAID intolerance

NSAID contraindication

79
Q

MOA of Colchicine

A

Prevents activation degranulation & migration of neutrophils associated with mediating some gout symptoms

80
Q

Pregnancy Category of Colchicine

A

Category C

81
Q

SE of Colchicine

A 
Diarrhea
N/V
Reversible peripheral neuropathy
Bone marrow suppression
Myopathy
82
Q

Dose Adjustment Needed in Colchicine

A 
>70 years old
CrCl less than 30 mL/min
Avoid in dialysis patients
Strong CYP3A4 inhibitors
Moderate CYP3A4 inhibitors
P-glycoprotein inhibitors
83
Q

Examples of Strong CYP 3A4 Inhibitors

A 
Clarithromycin
Itraconozaole
Ketoconazole
Nefazodone
HIV protease inhibitors
84
Q

Examples of Moderate CYP3A4 Inhibitors

A 
Diltiazem
Erythromycin
Fluconazole
Grape fruit juice
Verapamil
85
Q

Examples of P-Glycoprotein Inhibitors

A

Cyclosporine
Ranolazine
Amiodarone

86
Q

Contraindications to Colchicine

A

Renal impairment

Hepatic impairment

87
Q

No Relief of Symptoms on Colchicine After 24 Hours

A

+ glucocorticoid

Cautiously in conjunction with an NSAID

88
Q

Management Between Gout Attacks

A

Avoid thiazides & loop diuretics
Avoid niacin
Avoid aspirin

89
Q

Medications to Reduce Serum Uric Acid Indications

A

2+ episodes a year
Tophi
CKD Stage II+

90
Q

Allopurinol (Zyloprim)

A

Agent of choice for lowering rate
Xanthine oxidase inhibitor
Goal level: less than 6

91
Q

MOA of Allopurinol (Zyloprim)

A

Inhibits xanthine oxidase needed for eventual conversion of hypoxanthine to uric acid

92
Q

Necessary Dose Adjustment in Allopurinol (Zyloprim)

A

Renal Failure: less than 60 mL/min

93
Q

SE of Allopurinol (Zyloprim)

A 
Skin rash
Gout attack
Diarrhea
Nausea
Elevated liver enzymes
Hypersensitivity reactions
Bone marrow suppression
Hepatotoxicity
94
Q

2nd Line Therapy for Prevention of Gout

A

Probenecid

95
Q

MOA of Probenecid

A

Blocks tubular reabsorption of filtered rate & increases uric acid excretion by the kidney

96
Q

When is probenecid not effective?

A

CrCl less than 50 mL/min

97
Q

Contraindications of Probenecid

A

Hx of nephrolithiasis

98
Q

Prevention of Uric Acid Stones with Use of Probenecid

A

Increase fluid intake

Need agent to alkalinize the urine

99
Q

Other Medications that can Decrease Uric Acid Levels

A

Losartan
Fenofibrate
Vitamin C 500mg daily
Cherries

Rheumatology (8 decks)

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