Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CDM 2 > Exam 2: Gout > Flashcards

Exam 2: Gout Flashcards

1
Q

___ is the most common cause of inflammatory arthritis in the US

A

Gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hyperuricemia def

A

Elevated serum uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tophus def

A

A calculus containing sodium urate that develops around fibrous tissue around joins, typically in patients with gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Podagra def

A

A painful condition of the big toe caused by gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Uricase def

A

(Urate oxydase)
An enzyme that oxidatively degrades uric acid, thereby catalyzing conversion to soluble allantoin, which is much more soluble than uric acid. Found in most animals but NOT humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Uricosuric medications

A

Medications administered to increase the elimination of uric acid (usually 10% of uric acid is eliminated renally but meds increase it)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Uric Acid Pathway: Hypoxanthine becomes Xanthine via ___

A

Xanthine oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Uric Acid Pathway: ___ becomes Uric Acid via ___

A

Xanthine becomes UA via Xanthine Oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Uric acid is excreted by ___ in humans and metabolized via ___ in animals

A

Kidney in humans

Urate oxidase in animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Uric Acid Pathway: Uric acid becomes ____ via _____ in animals

A

Allatonin via urate oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Uric Acid Pathway: The uric acid metabolite, ____ ,is then excreted in the kidneys in ___

A

Allantoin

Animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Elevated SUA for men

A

> 7mg/dL (416µmol/L at 37º

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Elevated SUA for women

A

> 6mg/dL (357µmol/L) at 37º

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F: All pts with hyperuricemia develop acute gout flares

A

FALSE – if no gout, asymptomatic hyperuricemia does NOT require treatment

Not all pts with gout have hyperuricemia either!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Spectrum of Gout disease

A

Tophi (deposition of MSU in articular and extra-articular space)
Hyperuricemia
Recurrent acute arthritis attacks due to MSU crystals in synovial fluid
Interstitial renal disease (can lead to CKD)
Uric acid nephrolithiasis (kidney stones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which best describes gout?

  1. all pts with gout will progress to chronic tophaceous gout
  2. all pts with gout have hyperuricemia
  3. Pts with gout will have recurrent acute attacks separated by intercritical periods
  4. Gout is primarily due to the overproduction of uric acid
A
  1. Pts with gout will have recurrent acute attacks separated by intercritical periods – flares and then gets better and then worse and then better
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T/F: Developing countries have higher prevalence of gout than developed countries

A

FALSE – DEVELOPED > developing – remember RF: obesity, overindulgence in foods, HTN, HF, DM, sedentary lifestyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Risk factors of Gout

A 
Increasing age
M > F
Injury
Hyperuricemia 
Fasting
Recent surgery
Foods/drinks
Medications
Medical conditions
Genetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Risk factors: foods/drinks

A

High in purines (red meat)
Foods and drinks with high fructose corn syrup (soda, condiments)
Alcohol!! (both acute/chronic intake can increase SUA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Medication Risk factors: Overproduction

A

Cytotoxic chemotherapy (DNA breakdown, increase SUA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Medication Risk Facotrs: Underexcretion

A

Cyclosporine and tacro (RF kidney transplants)
Diuretics (loop/thiazide) – increased sodium reabsorption and UA , decreased volume in joints, increased UA saturation
Niacin
Low dose salicylates (<2g/day)
Pyrazinamide
Ethambutol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Medical Condition Risk Factors: Overproduction

A 
Myeloproliferative disorders
Lymphoproliferative disorders 
Malignancy 
Hemolytic disorders
Psoriasis 
Obesity
Tissue hypoxia 
Down syndrome
Glycogen storage diseases (Types III,V,VII)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Medical Condition Risk Factors: Underexcretion

A 
Chronic renal insufficiency 
Lead nephropathy
Volume depletion 
Diabetic or starvation ketoacidosis
Lactic acidosis
Obesity
Hyperparathyroidism
Hypothyroidism
Sarcoidosis
Chronic beryllium disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Genetic Risk Factors

A

HGPRT deficiency

PRPP over activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Treatment options for Acute Gouty Attacks

A

Colchicine, NSAIDs, Corticosteroids, and (IL1 antagonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Acute Gout presentation

A 
Monoarticular arthritis, redness/swelling/inflammation/warmth 
Fever
Elevated SUA 
Increased WBC 
MSU in synovial fluid 
Rapid onset
Overnight or after a trigger (alc, meats, diuretics) 
Excruciating pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

___ is the gold standard for definitive diagnosis of gout

A

evidence of MSU crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Pseudogout is related to ___ crystals while gout is related to ___ crystals

A

Pseudogout is calcium pyrophsophate crystals

Gout is MSU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

These 4 diagnoses can be similar to gout

A

Pseudogout
Septic arthritis
RA
Trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Acute Gout treatment goals

A

Rapid symptom relief
Prevent recurrent attacks
Prevent complications associated with chronic deposition of urate crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

T/F: Acute gout flares are not self-limiting

A

False - they are self-limiting (but very painful!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

All therapy should be initiated within ___ hours of acute gout symptom onset and continued for ____

A

within 24 hours

Continued for 1-2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Do NOT d/c ____ in an acute attack

A

ULT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Acute Gout treatment options: Self-care

A

Ice
Rest
Patient education

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

NSAIDs MOA

A

Peripheral inhibition of COX leading to inhibition of prostaglandin synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Acute Gout: NSAID: Adverse effects

A

Increased BP
Sodium/water retention
gastritis
GI Bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Acute Gout: NSAID: CI

A

Hx of NSAID allergy
HF
Renal sufficiency
Hx of GI ulcer/bleeds/perforations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Acute Gout: NSAIDs: DDI

A 
ACEI/ARB
Cyclosporine
Tacrolimus
Tenofovir
Lithium (can cause lithium toxicity - narrow therapeutic window) 
Anti-platelet and anticoag
Corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Acute Gout: NSAIDs monitoring

A 
S/sx of gout, reduced number for flares
CBC
LFT
SCR
Fecal occult blood test
Black tarry stools
BP
Edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Acute gout: Corticosteroids MOA

A

Synthetic glucocorticoid analog used for anti-inflammatory effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which corticosteroid is a good option of pts that have 1-2 joints affected by gout and it is locally administered?

A

Intra-articular triamcinolone acetonide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Acute gout: Corticosteroid ADEs

A

Acute: Hyperglycemia, leukocytosis, fluid retention, impaired wound healing, GI upset, insomnia, hypertension

Chronic: HPA axis suppression, osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Acute gout: Corticosteroid Precautions

A

Infection
DM
Peptic ulcer disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Acute gout: Corticosteroid DDIs

A

Strong CYP3A4 inhibitors
Fluoroquinolone
NSAIDs
Anti-hyperglycemic agents (DM meds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Acute gout: Corticosteroid Monitoring

A 
BG
BP
Mental status
Electrolytes
Edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Acute gout: Corticosteroid Pt education points

A

ADEs
Monitor glucose if pt with DM
Take with food/milk to minimize GI upset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Acute Gout: Colchicine MOA

A

May interfere with the intracellular assembly of the inflammasome complex present in neutrophils and monocytes that mediates the activation of interlukin-1β

Disruption of cytoskeletal functions through inhibition of β-tubulin polymerization into microtubules which prevents the activation, degranulation, and migration of neutrophils

**not completely sure how it works, essentially reduces inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Compare low and high doses of colchicine

A

Both gave pain relief but less ADEs with LOW dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Colchicine: PPX of gout flare dosing

A

0.6mg daily or BID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Colchicine: PPX Renal dosing adj?

A

CrCl <30 – 0.3mg daily

HD – 0.3mg twice WEEKLY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Colchicine: PPX Hepatic impairment dosing adj?

A

If severe, consider dose adj or alternative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Colchicine: Tx of acute gout flares dosing

A

1.2mg once then 0.6mg one hour later (max 1.8mg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Colchicine: Tx of Acute Gout Flare renal dosing adj?

A

No adjustment needed
If CrCl <30 – tx course should not be repeated more than once every 2 weeks
HD Single dose 0.6mg and treatment should not be repeated more than once every 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Colchicine: Tx of acute gout flares hepatic impairment dosing adj?

A

No adj needed

Severe – Tx courses should not be repeated more than once every 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Colchicine: In what situations should treatment courses not be repeated more than once every 2 weeks?

A

CrCl <30 (severe renal impairment)
HD
Severe hepatic impairment

56
Q

Colchicine: When should it NOT be used

A

Combined hepatic and renal impairment

57
Q

Colchicine ADEs

A 
GI: DIARRHEA, N/V, ab pain
Blood dyscrasias (myelosuppression, leukopenia, granulocytopenia, thrombocytopenia, aplastic anemia) 
Neuromuscular toxicity (myopathy, rhabdo, muscle weakness/pain)
58
Q

Colchicine: CI

A

Renal or hepatic impairment – do not use colchicine with PGP or strong CYP3A4 inhibitor
Combined renal and hepatic impairment–do not use Gloperba and Mitigare

59
Q

Colchicine brand names

A

Colcrys, Mitigare, Gloperba

60
Q

Colchicine: DDI

A

Substrate of CYP3A4 and PGP and Inducer of CYP2C8, 2C9, 2E1, 3A4
3A4 inhibitors: ritonavir, itraconazole, clarithromycin, ketoconazole, grapefruit juice, diltiazem, verapamil

PGP inhibitor: Ranolazine, cyclosporine

Statins and fibrates (increase risk of myalgia, won’t change dosing but monitor)

61
Q

Colchicine: Monitoring

A

CBC
S/sx of muscle toxicity
GI symptoms

62
Q

IL1-RA: Anakinra (Kineret) MOA

A

Competitively inhibits IL-1 from binding to the IL-1 receptor

63
Q

IL1-RA: Canakinumab (Illaris) MOA

A

Recombinant human anti-human interleukin-1 beta (IL1-B) monoclonal antibody of the IgG1/kappa isotype blocks IL-1 receptor interaction\

64
Q

IL1-RA: Rilonacept (Arcalyst) MOA

A

Acts as a decoy receptor that binds to IL-1 beta thereby blocking IL1-B interaction; also binds to IL-1 alpha and IL-1 receptor antagonist

65
Q

IL1-RA Agents (3)

A

Anakinra (Kineret)
Canakinumab (Illaris)
Rilonacept (Arcalyst)

66
Q

Anakinra brand name

A

Kineret

67
Q

Canakinumab brand name

A

Illaris

68
Q

Rilonacept brand name

A

Arcalyst

69
Q

IL1-RA: Adverse effects

A

Injection site reactions, neutropenia, hypersensitivity reactions, infectious disease

70
Q

IL1-RA: Contraindications

A

Hypersensitivity

71
Q

IL1-RA: DDI

A

Immunosuppressants (prof also mentioned live vaccines)

72
Q

IL-1RA Monitoring

A

Neurophil count, temperature, s/sx of infxn

73
Q

IL-1RA Pt education points

A

Report signs/symptoms of an infection, screen for TB infection prior to initiation, avoid live vaccines during therapy, side effects, proper injection technique, leave syringe at room temperature for 30 mins prior to injection (Anakinra)

74
Q

Acute Gout: Joint involvement - polyarticular def

A

≥4 joints w/arthritis involving more than 1 region (forefoot, midfoot, ankle/hindfoot, knee, hip, fingers, wrist, elbow, shoulder, other)

Acute gout attack involving 3 separate large joints

75
Q

Acute Gout: Mild severity range

A

≤4

76
Q

Acute Gout: Moderate severity range

A

5-6

77
Q

Acute Gout: Severe severity range

A

≥7

78
Q

Acute Gout: Early duration

A

<12h after onset

79
Q

Acute Gout: Well-established duration

A

12-36h after onset

80
Q

Acute gout: Late duration of gout

A

> 36h after attack onset (colchicine prob not effective at this time)

81
Q

Chronic Tophaceous Gout Presentation

A

Tophus: urate depostis

Fingers > olecranon bursae > forearm > achilles tendon > knees > wrists > hand

82
Q

Is Chronic Tophaceous Gout common?

A

late complication of gout, uncommon in the general pop

83
Q

Chronic Tophaceous Gout complications

A

Joint deformities and destruction
Pain
Damage to surrounding tissue
Nerve compression

84
Q

Chronic Gout: treatment goals

A

Maintain SUA <6
Reduce tissue level of uric acid
Dissolve existing urate crystals
Prevent further MSU crystal formation

85
Q

Chronic Gout: Initating ULT strongly recommended for

A

≥1 tophi

Radiographic damage attributable to gout

Frequent gout flares ≥2/year

86
Q

Chronic Gout: Initiating ULT conditionally recommended for

A

Pts with >1 flare but infrequent (<2/year)

Pts experiencing first flare and have CKD stage≥3, SUA >9, or urolithiasis (to prevent progression of disease)

87
Q

Chronic Gout: Initiating ULT conditionally recommended AGAINST

A

Pts with 1st flare with exceptions (sometimes pts get flares once and then never again)

Asymptomatic hyperuricemia

88
Q

You should ALWAYS start PPX (low dose NSAIDs/Colchicine/Steroids) prior to or with initiation of ___

A

ULT

89
Q

Mobilization Flares: PPX should be continued for at least ____

A

3-6 months

90
Q

ULT Clinical benefit

A

ULT can reduce flare frequency, resolve tophi, and reduce SUA conc

91
Q

Allopurinol brand name

A

Zylporim

92
Q

Allopurinol MOA

A

Xanthine oxidase inhibitors (reduces UA production)

93
Q

Allopurinol dosing

A

Start 50mg or 100mg po daily, titrate up by 50-100mg every 2-5 weeks until a goal of SUA <6

Doses >300 often given in divided doses, max dose 800mg/day

94
Q

Chronic Gout: Allopurinol renal dosing adj?

A

Initiation:
CKD stage ≥4 – 50mg
Everyone else – 100mg
≤100mg daily and lower for those with CKD
*renal adj only for intiation but not chronic use

Chronic: patients with CKD may require dose titration above 300mg/day to reach SU taget

95
Q

Chronic gout: allopurinol hepatic dose adj

A

No dose adj necessary

96
Q

Chronic Gout: Allopurinol metabolism

A

Hepatic to active metabolite (oxypurinol)

97
Q

What is the active metabolite of allopurinol?

A

Oxypurinol

98
Q

Chronic Gout: Allopurinol elimination

A

Renal

99
Q

Allopurinol ADE

A 
Hematologic (agranulocytosis, aplastic anemia, myelosuppression, thrombocytopenia) 
Renal failure
GI (Diarrhea, nausea)
Acute gout (mobilization flares)
Rash

ALLOPURINOL HYPERSENSITIVITY SYNDROME (AHS)

100
Q

Chronic Gout: Allopurinol: AHS prevention

A

HLA-B*5801 screening

101
Q

Chronic Gout: Allopurinol: AHS manifestation

A

Rash chills fever leukopenia leukocytosis eosinophilia and pruritus
May be severe and FATAL (hepatotoxicity, vasculitis, SJS, and TEN)

102
Q

Chronic Gout: Allopurinol: AHS management

A

D/C allopurinol at first sign of rash

Supportive care

103
Q

Chronic Gout: Allopurinol CI

A

allopurinol sensitivity

Concurrent didanosine

104
Q

Chronic Gout: Allopurinol DDI

A 
Azathioprine and 6MP (MUST reduce dose of azathioprine and 6MP when used with allopurinol) 
Didanosine
Theophylline
Pegloticase
Loop/thiazide diuretics
105
Q

Chronic Gout: Allopurinol monitoring

A

HLA-B*5801 prior to initiation in high-risk subpopulations (han chinese, korean, thai, or AA) SCR, CBC, LFTs, rash

106
Q

Chronic Gout: Febuxostat MOA

A

Non-purine inhibitor of xanthine oxidase (XOI) leading to reduced production of uric acid

107
Q

Febuxostat brand name

A

Uloric

108
Q

Chronic Gout: Febuxostat dosing

A

Initiate at 40mg po daily; if goal SUA is not achieved by 2 weeks, increase to 80mg po daily, max dose 80mg in US

109
Q

Chronic Gout: Febuxostat renal/hepatic dosing adj

A

None for mild-moderate impairment

Max 40mg with severe renal impairment

110
Q

Chronic Gout: Febuxostat ADE

A

Abnormal LFTs
Nausea
Gout flares due to mobilization
Arthralgia, rash

111
Q

Chronic gout: Febuxostat CI

A

Concomitant use of azathioprine or 6MP

112
Q

Chronic gout: Febuxostat precaution

A

Acute gout flare
Cardiovascular events (BBW)
Hepatotoxicity
Serious skin reactions

113
Q

Comparing XOI, which is the preferred first-line agent?

A

Allopurinol

114
Q

Probenecid MOA

A

Competitively inhibits the postsecretory renal proximal tubular reabsorption of uric acid

115
Q

Probenecid dosing

A

500g po daily or BID, titrated up to 500-2000mg/day

116
Q

Probenecid brand name

A

Benamid

117
Q

Probenecid renal dosing adj?

A

AVOID – CrCl <50

118
Q

Probenecid ADES

A

Flushing
Dizziness, fever, headache
Alopecia, dermatitis, pruritus, rash
Anorexia, dyspepsia, GERD, nausea
Anemia aplastic anemia, hemolytic anemia (in G6PD deficiency), leukopenia
Precipitation of acute gouty arthritis
Rash, hypersensitivity, uric acid nephrolithiasis

119
Q

Probenecid contraindication

A 
Hx of urolithiasis
overproducers of uric acid
Hypersensitivity to probenecid
Small or large dose salicylate therapy
Blood dyscasias 
<2 yo 
Initiation during acute gout attack
120
Q

Probenecid precautions

A

G5PD, PUD, renal impairment

Methotrexate, penicillin, salicylates

121
Q

Probenecid DDI

A

Salicylates
Penicillins/cephalosporins/carbapenems
Methotrexate
Pegloticase

122
Q

Probenecid monitoring

A

SUA

Renal fxn

123
Q

Probenecid pt education pts

A

Increase fluid intake

124
Q

Uricosurics examples

A

Probenecid (Benemid)

Losartan

125
Q

Losartan gout dosing and place in therapy

A

No specific dosing for gout

If pt has HTN, add on to XOI to pts not controlled on single agent

126
Q

Probenecid place in therapy

A

XOI is preferred with CKD ≥3

Can be ADD-ON

127
Q

Pegloticase brand name

A

Krystexxa

128
Q

Pegloticase MOA

A

pegylated recombinant modified mammalian urate oxidase (uricase)

129
Q

Pegloticase is usually administered with __ and ___ as pre-medication

A

corticosteroid and antihistamine

130
Q

Pegloticase ADEs

A 
Gout flares
Infusion reactions
Nausea
Vomiting
Bruising
Nasopharyngitis
Constipation
Chest pain
Anaphylaxis
131
Q

Pegloticase boxed warning

A

Anaphylaxis (usually within 2 hrs)

132
Q

Pegloticase CI

A

G5PD deficiency

133
Q

Pegloticase precautions

A

Anaphylaxis
Infusion reactions (slow it down)
Gout flares
Congestive HF

134
Q

Pegloticase DDI

A

No studies with other drugs have been done – stop ALL other ULT when you initiate pegloticase

135
Q

T/F: You can use pegloticase as monotherapy or dual add-on therapy

A

FLASE – pegloticase is monotherapy ONLY, STOP all other ULT when you initiate pegloticase

136
Q

Pegloticase monitoring

A

SUA levels, freq of gout flares
SUA levels
G6PD screening prior to initiation in high risk pt pops (AA and mediterranean ancestry)
S/sx of anaphylaxis

137
Q

Pegloticase pt education

A

ADEs (gout flares, nasopharyngitis, etc.)

S/sx of infusion rxn or anaphylaxis

CDM 2 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions