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Clin Med semester 2 > Rheumatology- Paulson (exam 2) > Flashcards

Rheumatology- Paulson (exam 2) Flashcards

1
Q

Gout S/Sx: (Pts may have:)

A
  • Hyperuricemia
  • Recurring attacks of acute arthritis
  • Tophi
  • Renal disease
  • Uric acid nephrolithiasis
  • Chronic deforming arthritis
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2
Q

What are tophi?

A

deposits of monosodium urate monohydrate crystals)

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3
Q

Gout: Epidemiology/RF?

A
  • Men > Women (90% are men). Men: 40-60. Women: after 60.
  • Pacific Islanders (Filipinos, Samoans)
  • ALCOHOL (especially beer)
  • OBESITY
  • Genetic in some
  • Foods that promote hyperuricemia
  • Chronic diseases
  • Medications
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4
Q

Gout: What foods may promote hyperuricemia?

A
  • Red meat
  • Seafood
  • Fructose
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5
Q

Gout: What food is protective for hyperuricemia?

A

Dairy products

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6
Q

Gout: Which medications affect urate balance?

A
  • Thiazides
  • Loop diuretics
  • Low-dose ASA
  • Cyclosporine
  • Niacin
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7
Q

Gout pathophysiology: Serum urate levels for hyperuricemia?

A

> 6.8 mg/dL

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8
Q

(T/F) For gout to result from hyperuricemia, serum urate levels are typically above 6.8 mg/dL prior to the onset of gout S/Sx.

A
  • False. Especially rapid fluctuations in serum levels can precipitate S/Sx.
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9
Q

T/F: To dx a Pt with gout, they must have hyperuricemia

A

False. Hyperuricemia needed (but hyperuricemia ≠ gout)

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10
Q

For gout, _______ level has to be high enough for crystals to precipitate

A

monosodium urate (MSU)

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11
Q

Gout: How does resolution of acute inflammation occur?

A
  • Mediated by immune mechanisms (even without treatment)
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12
Q

Gout: long term Complications?

A
  • Chronic inflammatory process which has an effect on osteoclasts, blasts, and chondrocytes that contribute to tophi formation, erosion of bone, and joint injury.
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13
Q

Uric acid is the end product of ______ metabolism

A

purine

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14
Q

When considering uric acid balance, what are the two major categories?

A
  • Underexcreters

- Overproducers

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15
Q

Uric acid balance: Which group is more common, underexcreters or overproducers?

A
  • Underexcreters
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16
Q

Conditions associated with being an underexcreter?

A
  • Renal insufficiency
  • Acidosis (ie: diabetic ketoacidosis, ketogenic diet, lactic acidosis)
  • Volume depletion/dehydration
  • Lead exposure
  • Medications
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17
Q

Uric acid balance: Which medications can make one under-excrete uric acid?

A
  • **Low-dose ASA
  • ** Thiazides
  • **Loop diuretics
  • Nicotinic acid
  • Cyclosporine
  • Levodopa
  • Ethambutol
  • Pyrazinamide
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18
Q

Uric acid balance: What conditions can make one overproduce uric acid?

A
  • Inherited defect of metabolism
  • Myeloproliferative and lymphoproliferative disorders, polycythemia, carcinoma–> Tumor lysis syndrome
  • Chronic hemolytic anemias
  • Transient hyperuricemia associated with ATP consumption.
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19
Q

Uric acid balance: What inherited defect of metabolism can lead to an overproduction of uric acid?

A
  • Lesch-Nyhan syndrome

- Kelley-Seegmiller syndrome

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20
Q

Uric acid balance: What are examples of transient hyperuricemia associated with ATP consumption?

A
  • Strenuous exercise
  • Status epilepticus
  • MI
  • Sepsis
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21
Q

Gout: What are the 3 stages of gout?

A

1) Acute gouty arthritis
2) Intercritical (Interval) gout
3) Chronic articular and tophaceous gout.

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22
Q

Acute Gouty Arthritis- Chief complaint/Hx

A
  • “My big toe hurts”
  • Sudden onset, often at night
  • Severely painful and tender, swollen joint, red, warm
  • May complain of fever
  • Reaches maximal severity in about 12-24 hours
  • May have history of similar attacks prior
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23
Q

Acute gouty arthritis: PE findings?

A
  • Swollen, very tender, red and warm overlying skin.
  • (+/-) desquamation
  • (+/-) Tophi
  • (+/-) Podagra
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24
Q

Acute gouty arthritis: MC site?

A
  • MTP of great toe is classic
  • “Podagra”
  • *Usually monoarticular and in the lower extremity
  • *Polyarticular is possible (usually later flares)
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25
Q

What physical exam finding is pathognomonic for gout?

A

tophi (Irregular, asymmetric macroscopic deposits of urate)

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26
Q

Common sites for tophi?

A
  • External ear
  • Hands
  • Olecranon
  • Feet
  • Knee
  • Achilles tendon
  • Forearm
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27
Q

Gout: Are tophi painful?

A
  • Usually painless (but can become acutely inflamed)

- - Usually develop after years.

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28
Q

Gout: How can tophi be destructive over the sites they are found?

A
  • Maintains a state of inflammation

- Promote tissue and joint destruction around them.

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29
Q

Renal complications of gout?

A
  • **Uric acid nephrolithiasis
  • **Chronic urate nephropathy
  • Uric acid nephropathy
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30
Q

How can gout cause chronic urate nephropathy?

A

MSU crystals are deposited in the renal medulla and pyramids

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31
Q

Describe nephropathy

A

Nephropathy is a disease of the kidneys caused by damage to the small blood vessels or to the units in the kidneys that clean the blood.

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32
Q

How does gout cause uric acid nephropathy?

A
  • Acute renal failure (ARF) when large amounts of uric acid and crystals precipitate in the collecting ducts and ureters.
  • Usually seen as part of tumor lysis syndrome
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33
Q

DDx of acute gout?

A
  • Septic arthritis
  • Trauma
  • Calcium pyrophosphate crystal deposition (CPPD) disease (pseudogout)
  • Cellulitis
  • Rheumatoid arthritis
  • Lyme disease
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34
Q

DDx of chronic gout?

A
  • Osteoarthritis
  • Rheumatoid arthritis
  • Psoriatic arthritis
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35
Q

Gout: Labs & Imaging for Dx?

A
  • Synovial fluid analysis
  • U/S
  • Radiographs
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36
Q

What would you find in an aspirate of synovial fluid (analysis)? KNOW

A
  • Monosodium urate crystals

- “Negatively birefringent”, needle-like, when viewed with polarized light microscopy. KNOW!!

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37
Q

Gout labs: U/S findings?

A
  • Hyperechoic linear density (double contour sign) over the joint cartilage or deposits that look like tophi (hypoechoic cloudy area)`
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38
Q

Gout labs: Radiograph findings?

A
  • “Rat bite” lesions later in disease process

- If next to a tophus = gout.

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39
Q

Gout labs: Additional labs?

A
  • Serum uric acid (often elevated in most Pts during an attack)
  • Peripheral WBC (can be high)
  • ESR/CRP (can be elevated)
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40
Q

Gout Tx: If PT is asymptomatic but has hyperuricemia?

A

Don’t treat

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41
Q

Gout Tx: Lifestyle modifications?

A
  • Lose weight
  • Reduce alcohol consumption
  • Reduce purine-rich food consumption
  • Drink enough fluids to urinate >-2L per day
  • Avoid hyperuricemic meds, if possible.
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42
Q

Gout Tx: Tx goal?

A
  • Relieve the patient’s pain as quickly as possible.

- Keep in mind comorbidities when selecting meds

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43
Q

Gout Tx: (T/F) urate-lowering medications are the medications that can help the patient’s pain management in acute attacks.

A

False! they don’t help in acute attacks- don’t start one during acute attack

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44
Q

Gout Tx: What is an example of a common urate-lowering medication?

A

Allopurinol

45
Q

Gout Tx: If a patient is on a urate-lowering medication and a gout flare-up occurs, should they discontinue that medication for the duration of the flare-up?

A
  • No

- Continue as prescribed.

46
Q

Gout Tx: What is the 1st line medication for an acute attack?

A
  • NSAIDs
47
Q

Gout Tx: Examples of common NSAIDs for an acute attack?

A
  • Naproxen
  • Indomethacin
  • Celecoxib (Celebrex)
48
Q

Gout Tx: How do you direct a patient to take an NSAID?

A
  • Discontinue 1-2 days after complete clinical resolution.

- (Typical course might be 5-7 days)

49
Q

Gout Tx: Contraindications to NSAID usage for acute attacks?

A
  • CKD with CrCl < 60
  • Active ulcer
  • NSAID allergy
  • Concurrent use of anticoagulant
  • CV disease (esp. uncontrolled CHF or HTN)
50
Q

Gout Tx: What is one of the best antigout medications used in acute attacks in patients who cannot take NSAIDs?

A

Colchicine

51
Q

Gout Tx: When should a patient start taking colchicine?

A

Within 12-24 hours of symptoms

52
Q

Gout Tx: Colchicine administration instructions? Doseage?

A
  • DAY 1: 1.2 mg initially, then 0.6 mg 1 hour later.
  • DAY 2 (& onward) 0.6 mg QD-BID
  • d/c 2-3 days after symptoms have resolved.
53
Q

Gout Tx: Common S/E of colchicine?

A
  • Diarrhea
  • Abdominal cramping
  • Reversible peripheral neuropathy may be seen
54
Q

Gout Tx: Contraindications to colchicine?

A
  • Severe hepatic impairment
  • Severe renal impairment
  • Concomitant use of a mod-strong inhibitor of P-gp and/or CYP3A4 inhibitor
55
Q

Gout Tx: When are corticosteroids a good option?

A
  • Good for people who can’t take NSAIDs or colchicine
56
Q

Gout Tx: How could you administer the corticosteroid during an acute attack? (routes and medication name)

A
  • Intra-articular injection: triamcinolone 40 mg (large joint), 30 mg for a medium joint, or 10 mg for a small joint
  • Oral: prednisone 40-60 mg/day tapered over 7 days
  • IV: methylprednisolone 40 mg/day tapered over 7 days
  • IM: triamcinolone 40-60 mg. May need to repeat 1-2x.
57
Q

Gout Tx: Conditions that may be problematic with a corticosteroid plan?

A
  • CHF
  • Glucose intolerance (**dont use in diabetic pts)
  • Poor control of HTN
58
Q

Preventative Gout Tx: At what stage of gout would you address preventative measures?

A

During the intercritical period

59
Q

Preventative Gout Tx: Goal?

A
  • To achieve a serum urate level <6 mg/dL

- Slowly (not more than 1-2 mg/dL/month)

60
Q

Preventative Gout Tx: Indications for urate-lowering medications?

A
  • Frequent gout attacks
  • Tophi
  • Clinical or radiographic signs of chronic gouty arthropathy
  • Gout with renal insufficiency
  • Recurrent uric acid nephrolithiasis
  • Premenopausal women or men <25 with urinary uric acid excretion >1100 mg/day
61
Q

Preventative Gout Tx: When initiating antihyperuricemic therapy, what else do you have to consider?

A
  • Use low-dose prophylactic colchicine (or low-dose NSAID) when initiating antihyperuricemic therapy to reduce risk for acute flare.
62
Q

Preventative Gout Tx: Why should you use low-dose prophylactic colchicine (or low-dose NSAID) when initiating antihyperuricemic therapy?

A

To reduce risk for acute flare.

63
Q

Preventative Gout Tx: What is the class of medication most commonly used to prevent gout flare-ups?

A

Xanthine oxidase inhibitors (XOI)

64
Q

Preventative Gout Tx: What are the two main XOI medications used?

A
  • Allopurinol

- Febuxostat

65
Q

XOI: Action of these medications?

A
  • Reduce production of uric acid.
66
Q

XOI: Dosage and instructions for initiating allopurinol?

A
  • Start at 100mg/day

- Titrate up every 2-5 weeks

67
Q

XOI: Most people who take allopurinol require what dosage a day?

A

≥300 mg/day

68
Q

XOI: When would you reduce the recommended initial dose of allopurinol in a patient?

A

In PTs with CKD

69
Q

XOI: When initiating allopurinol, what other medication should you also initiate?

A
  • Prophylactic colchicine (OR)

- Low-dose NSAID

70
Q

XOI: S/E of allopurinol?

A

rash, including severe cutaneous reactions/TEN (especially in Asian patients, those with HLA-B*5801 allele)

-(Toxic epidermal necrolysis (TEN) is a rare, life-threatening skin reaction, usually caused by a medication. It’s a severe form of Stevens-Johnson syndrome (SJS).)

71
Q

XOI: Febuxostate initial dosage?

A
  • Start at 40mg/day and titrate up to 80mg after 2 weeks.
72
Q

XOI: When initiating Febuxostat, what other medication do you want to initiate?

A
  • Prophylactic colchicine (OR)

- Low-dose NSAID

73
Q

XOI: S/E of febuxostat?

A
  • Less hypersensitivity reactions

- Can develop abnormal LFTs, and slightly higher rate of cardiovascular events

74
Q

Gout Tx: Describe uricosuric medications.

A
  • Block tubular reabsorption of urate and increases the rate that uric acid is renally excreted.
75
Q

Gout Tx: When considering initiating a uricosuric medication, what baseline lab would you consider having?

A
  • The PT must have normal renal function (CrCl > 60)
76
Q

Gout Tx: When a patient initiates uricosuric medications, what do you need to advise the patient of?

A
  • Urinate at least 2L/day to avoid precipitation of uric acid in urinary tract.
77
Q

Gout Tx: Common uricosuric medication? and S/E?

A 
*Probenecid 
S/E: - Rash
- Precipitation of acute gout
- GI intolerance
- Uric acid stone formation
78
Q

Gout Tx: Uricosuric medications are contraindicated in which patients?

A
  • renal hypofunction (CrCl<60)

- **PTs with G6PD

79
Q

Gout Tx: When would you consider treating a patient with uricase?

A
  • For patients who have been refractory to all other therapies.
80
Q

Gout Tx: Describe uricase.

A

An enzyme present in other mammals that breaks urate down to allantoin, which is more easily excreted.

81
Q

Gout Tx: Common uricase medication?

A
  • Pegloticase: given IV every 2 weeks
82
Q

Gout Tx: What special considerations need to be made before starting a uricase therapy?

A
  • Need to have premedication for infusion reactions and have gout flare prophylaxis for the first 6 months of therapy.
83
Q

Gout Tx: Uricase is contraindicated in which patients?

A
  • PTs with G6PD deficiency.
84
Q

Gout Tx: How do you choose your treatment?

A
  • 24-hour urine uric acid test.

- Determine if the patient is an undersecreter of uric acid or an overproducer of uric acid.

85
Q

Gout Tx: When looking at the results of a 24-hour urine uric acid test, what is the lab value point that separates undersecreters from overproducers?

A

<800 mg/dL–> they are an undersecreter of uric acid

> 800 mg/d–> they are an overproducer

In both cases give them an XOI
-if they fail XOI–> give uricase
Give allopurinol!! best choice

86
Q

Gout Tx: Interpret a 24-hour urine uric acid test of 922 mg/dL

A
  • Overproducer
87
Q

Gout Tx: Interpret a 24-hour urine uric acid test of 700 mg/dL

A
  • Undersecreter
88
Q

Prognosis/Referral:

-what should you educate the Pt on regarding acute gouty attacks?

A
  • Acute attack will self-resolve even without treatment
  • Over time, attacks will become more frequent and last longer
  • The younger a patient is at initial presentation, the more likely to have a progressive course
  • With urate-lowering meds, much less chronic gouty arthritis, tophi, and deformity
  • -Can refer to rheumatology
  • Follow up
89
Q

Describe Pseudogout

A

-Also known as calcium pyrophosphate dihydrate (CPPD or CPP) deposition disease, chondrocalcinosis, or pyrophosphate arthropathy

=Arthropathy caused by precipitation of calcium pyrophosphate dihydrate crystals that can cause acute, recurrent, or chronic arthritis which can mimic gout.

90
Q

Chondrocalcinosis=

A

Radiographic evidence of calcification in articular cartilage

91
Q

Risk factors for Pseudogout

A
  • Older adults, both men and women
  • Increases in prevalence with increasing age
  • Rare before 55.
  • Around 50% of those >85 are affected
  • Joint trauma
  • Familial chondrocalcinosis
  • Hemochromatosis
92
Q

Most CPPD (aka pseudogout) is _____

A

idiopathic

–but Early-onset familial CPPD with chromosomal linkages

93
Q

Describe the pathophysiology of CPPD

A
  1. Excess pyrophosphate production in cartilage–> calcium pyrophosphate supersaturation–> CPP crystals are formed/deposited
  2. The CPP crystal is felt to be involved in joint inflammation
  3. Inflammation triggered by CPPD degrades cartilage
94
Q

Clinical Sx of CPPD (2 types)

A
  • asymptomatic

- Acute arthritis/pseudogout

95
Q

Asymptomatic CPPD Pt lab findings

A

May see CPP deposition in a joint on a radiograph but have no symptoms

96
Q

Acute Arthritis/pseudogout Sx

A
  • Self-limited, sudden attacks of pain, redness, warmth, disability, and swelling, monoarticular or oligoarticular
  • *Knee is most commonly affected.
  • Others: wrists, shoulders, elbows, ankles
  • Can be provoked by surgery (esp. parathyroidectomy), trauma, or major illness
  • May have associated fever/chills
97
Q

Chronic CPP crystal inflammatory arthritis (“pseudo-RA”) - describe this disorder

A

-Inflammatory arthritis where CPP crystals can be found in joint fluid
-Similar Sx to RA, involving multiple joints in a symmetric patterns
-Usually affects joints unaffected by OA
MCPs, wrists, elbows, glenohumeral joints
-Asynchronous waxing and waning of inflamed joints

98
Q

OA with CPPD (“pseudo-OA”)

Describe this disorder

A

About half of symptomatic patients have progressive joint degeneration

  • -Knees most common. Also wrists, MCPs, hips, shoulders, elbows, spine
  • -Clinical exam like that of OA (tenderness, bony enlargement, crepitus, restriction of motion)
99
Q

Pseudo-neuropathic joint disease

A

=Severe joint degeneration from CPP crystal deposition

  • Resembles neuropathic arthropathy
  • Unlike neuropathic arthropathy, there is not usually any neurologic impairment
100
Q

DDx for Acute arthritis/pseudogout

A

Gout
Septic arthritis
Trauma
Lyme disease

101
Q

DDx for Chronic CPP

A

Osteoarthritis
Rheumatoid Arthritis
Peripheral spondyloarthritis
Neuropathic arthropathy

102
Q

Dx: Lab findings for CPPD

A
  • *CPP crystals in joint aspirate are diagnostic
  • **“weakly positively birefringent rhomboid crystals” by polarized light microscopy
  • Radiographic evidence of chondrocalcinosis:
  • -Linear and punctate densities within hyaline or articular cartilage
  • -Often see degenerative changes (subchondral cysts, osteophyte formation, fragmentation of bone and cartilage)
103
Q

Tx Acute pseudogout

A
  • Aspiration then intraarticular glucocorticoid injection–>Triamcinolone
  • NSAIDs: Indomethacin, naproxen, salicylates
  • Colchicine
  • Systemic corticosteroids (oral, IV, or IM)
104
Q

Tx OA with CPPD

A

Treat like OA

105
Q

Tx Pseudo-neuropathic joint disease

A

treat like charcot arthropathy

106
Q

When should you consider Prophylaxis tx for CPPD?

A

Consider if the patient has ≥3 attacks per year
–>Colchicine 0.6 mg PO BID
If this doesn’t work or the patient is intolerant, could use an NSAID instead.

107
Q

Pseudo-RA prophylaxis:

A

NSAIDs 1st choice (use lowest dose possible): Naproxen, or Indomethacin

  • -Alternatives if NSAIDs ineffective:
  • Colchicine 0.6 mg QD or BID
  • Hydroxychloroquine
  • Low-dose glucocorticoids ie: prednisone (up to 10 mg /day)
108
Q

Prognosis/Referral: CPPD

A

Attacks will resolve even without treatment
Can cause chronic symptoms
Can refer to rheumatology

109
Q

Compare & contrast Gout and CPPD Arthropathy

A

Gout: middle aged men and elderly men. Joints: MTP, ankles, knees. Dx: Tophi present. Crystals: needle-shaped and strongly negative birefringent

CPPD arthopathy: elderly men and women. Joints: knees MC!! and wrists. NO tophi present. Radiography: Chondrocalcinosis. Crystals: small, rhomboid shaped or weakly positive birefringent

Clin Med semester 2 (24 decks)

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