Rheumatology- Paulson (exam 2) Flashcards
(109 cards)
1
Q
Gout S/Sx: (Pts may have:)
A
- Hyperuricemia
- Recurring attacks of acute arthritis
- Tophi
- Renal disease
- Uric acid nephrolithiasis
- Chronic deforming arthritis
2
Q
What are tophi?
A
deposits of monosodium urate monohydrate crystals)
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
4
Q
Gout: What foods may promote hyperuricemia?
A
- Red meat
- Seafood
- Fructose
5
Q
Gout: What food is protective for hyperuricemia?
A
Dairy products
6
Q
Gout: Which medications affect urate balance?
A
- Thiazides
- Loop diuretics
- Low-dose ASA
- Cyclosporine
- Niacin
7
Q
Gout pathophysiology: Serum urate levels for hyperuricemia?
A
> 6.8 mg/dL
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.
9
Q
T/F: To dx a Pt with gout, they must have hyperuricemia
A
False. Hyperuricemia needed (but hyperuricemia ≠ gout)
10
Q
For gout, _______ level has to be high enough for crystals to precipitate
A
monosodium urate (MSU)
11
Q
Gout: How does resolution of acute inflammation occur?
A
- Mediated by immune mechanisms (even without treatment)
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.
13
Q
Uric acid is the end product of ______ metabolism
A
purine
14
Q
When considering uric acid balance, what are the two major categories?
A
- Underexcreters
- Overproducers
15
Q
Uric acid balance: Which group is more common, underexcreters or overproducers?
A
- Underexcreters
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
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
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.
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
20
Q
Uric acid balance: What are examples of transient hyperuricemia associated with ATP consumption?
A
- Strenuous exercise
- Status epilepticus
- MI
- Sepsis
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.
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
23
Q
Acute gouty arthritis: PE findings?
A
- Swollen, very tender, red and warm overlying skin.
- (+/-) desquamation
- (+/-) Tophi
- (+/-) Podagra
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)
25
What physical exam finding is pathognomonic for gout?
tophi (Irregular, asymmetric macroscopic deposits of urate)
26
Common sites for tophi?
- External ear
- Hands
- Olecranon
- Feet
- Knee
- Achilles tendon
- Forearm
27
Gout: Are tophi painful?
- Usually painless (but can become acutely inflamed)
| - - Usually develop after years.
28
Gout: How can tophi be destructive over the sites they are found?
- Maintains a state of inflammation
| - Promote tissue and joint destruction around them.
29
Renal complications of gout?
- **Uric acid nephrolithiasis
- **Chronic urate nephropathy
- Uric acid nephropathy
30
How can gout cause chronic urate nephropathy?
MSU crystals are deposited in the renal medulla and pyramids
31
Describe nephropathy
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.
32
How does gout cause uric acid nephropathy?
- 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
33
DDx of acute gout?
- Septic arthritis
- Trauma
- Calcium pyrophosphate crystal deposition (CPPD) disease (pseudogout)
- Cellulitis
- Rheumatoid arthritis
- Lyme disease
34
DDx of chronic gout?
- Osteoarthritis
- Rheumatoid arthritis
- Psoriatic arthritis
35
Gout: Labs & Imaging for Dx?
- Synovial fluid analysis
- U/S
- Radiographs
36
What would you find in an aspirate of synovial fluid (analysis)? KNOW
- Monosodium urate crystals
| - "Negatively birefringent", needle-like, when viewed with polarized light microscopy. KNOW!!
37
Gout labs: U/S findings?
- Hyperechoic linear density (double contour sign) over the joint cartilage or deposits that look like tophi (hypoechoic cloudy area)`
38
Gout labs: Radiograph findings?
- "Rat bite" lesions later in disease process
| - If next to a tophus = gout.
39
Gout labs: Additional labs?
- Serum uric acid (often elevated in most Pts during an attack)
- Peripheral WBC (can be high)
- ESR/CRP (can be elevated)
40
Gout Tx: If PT is asymptomatic but has hyperuricemia?
Don't treat
41
Gout Tx: Lifestyle modifications?
- Lose weight
- Reduce alcohol consumption
- Reduce purine-rich food consumption
- Drink enough fluids to urinate >-2L per day
- Avoid hyperuricemic meds, if possible.
42
Gout Tx: Tx goal?
- Relieve the patient's pain as quickly as possible.
| - Keep in mind comorbidities when selecting meds
43
Gout Tx: (T/F) urate-lowering medications are the medications that can help the patient's pain management in acute attacks.
False! they don’t help in acute attacks- don’t start one during acute attack
44
Gout Tx: What is an example of a common urate-lowering medication?
Allopurinol
45
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?
- No
| - Continue as prescribed.
46
Gout Tx: What is the 1st line medication for an acute attack?
- NSAIDs
47
Gout Tx: Examples of common NSAIDs for an acute attack?
- Naproxen
- Indomethacin
- Celecoxib (Celebrex)
48
Gout Tx: How do you direct a patient to take an NSAID?
- Discontinue 1-2 days after complete clinical resolution.
| - (Typical course might be 5-7 days)
49
Gout Tx: Contraindications to NSAID usage for acute attacks?
- CKD with CrCl < 60
- Active ulcer
- NSAID allergy
- Concurrent use of anticoagulant
- CV disease (esp. uncontrolled CHF or HTN)
50
Gout Tx: What is one of the best antigout medications used in acute attacks in patients who cannot take NSAIDs?
Colchicine
51
Gout Tx: When should a patient start taking colchicine?
Within 12-24 hours of symptoms
52
Gout Tx: Colchicine administration instructions? Doseage?
- 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
Gout Tx: Common S/E of colchicine?
- Diarrhea
- Abdominal cramping
- Reversible peripheral neuropathy may be seen
54
Gout Tx: Contraindications to colchicine?
- Severe hepatic impairment
- Severe renal impairment
- Concomitant use of a mod-strong inhibitor of P-gp and/or CYP3A4 inhibitor
55
Gout Tx: When are corticosteroids a good option?
- Good for people who can't take NSAIDs or colchicine
56
Gout Tx: How could you administer the corticosteroid during an acute attack? (routes and medication name)
- 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
Gout Tx: Conditions that may be problematic with a corticosteroid plan?
- CHF
- Glucose intolerance (**dont use in diabetic pts)
- Poor control of HTN
58
Preventative Gout Tx: At what stage of gout would you address preventative measures?
During the intercritical period
59
Preventative Gout Tx: Goal?
- To achieve a serum urate level <6 mg/dL
| - Slowly (not more than 1-2 mg/dL/month)
60
Preventative Gout Tx: Indications for urate-lowering medications?
- 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
Preventative Gout Tx: When initiating antihyperuricemic therapy, what else do you have to consider?
- Use low-dose prophylactic colchicine (or low-dose NSAID) when initiating antihyperuricemic therapy to reduce risk for acute flare.
62
Preventative Gout Tx: Why should you use low-dose prophylactic colchicine (or low-dose NSAID) when initiating antihyperuricemic therapy?
To reduce risk for acute flare.
63
Preventative Gout Tx: What is the class of medication most commonly used to prevent gout flare-ups?
Xanthine oxidase inhibitors (XOI)
64
Preventative Gout Tx: What are the two main XOI medications used?
- Allopurinol
| - Febuxostat
65
XOI: Action of these medications?
- Reduce production of uric acid.
66
XOI: Dosage and instructions for initiating allopurinol?
- Start at 100mg/day
| - Titrate up every 2-5 weeks
67
XOI: Most people who take allopurinol require what dosage a day?
≥300 mg/day
68
XOI: When would you reduce the recommended initial dose of allopurinol in a patient?
In PTs with CKD
69
XOI: When initiating allopurinol, what other medication should you also initiate?
- Prophylactic colchicine (OR)
| - Low-dose NSAID
70
XOI: S/E of allopurinol?
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
XOI: Febuxostate initial dosage?
- Start at 40mg/day and titrate up to 80mg after 2 weeks.
72
XOI: When initiating Febuxostat, what other medication do you want to initiate?
- Prophylactic colchicine (OR)
| - Low-dose NSAID
73
XOI: S/E of febuxostat?
- Less hypersensitivity reactions
| - Can develop abnormal LFTs, and slightly higher rate of cardiovascular events
74
Gout Tx: Describe uricosuric medications.
- Block tubular reabsorption of urate and increases the rate that uric acid is renally excreted.
75
Gout Tx: When considering initiating a uricosuric medication, what baseline lab would you consider having?
- The PT must have normal renal function (CrCl > 60)
76
Gout Tx: When a patient initiates uricosuric medications, what do you need to advise the patient of?
- Urinate at least 2L/day to avoid precipitation of uric acid in urinary tract.
77
Gout Tx: Common uricosuric medication? and S/E?
```
*Probenecid
S/E: - Rash
- Precipitation of acute gout
- GI intolerance
- Uric acid stone formation
```
78
Gout Tx: Uricosuric medications are contraindicated in which patients?
- renal hypofunction (CrCl<60)
| - **PTs with G6PD
79
Gout Tx: When would you consider treating a patient with uricase?
- For patients who have been refractory to all other therapies.
80
Gout Tx: Describe uricase.
An enzyme present in other mammals that breaks urate down to allantoin, which is more easily excreted.
81
Gout Tx: Common uricase medication?
- Pegloticase: given IV every 2 weeks
82
Gout Tx: What special considerations need to be made before starting a uricase therapy?
- Need to have premedication for infusion reactions and have gout flare prophylaxis for the first 6 months of therapy.
83
Gout Tx: Uricase is contraindicated in which patients?
- PTs with G6PD deficiency.
84
Gout Tx: How do you choose your treatment?
- 24-hour urine uric acid test.
| - Determine if the patient is an undersecreter of uric acid or an overproducer of uric acid.
85
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?
<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
Gout Tx: Interpret a 24-hour urine uric acid test of 922 mg/dL
- Overproducer
87
Gout Tx: Interpret a 24-hour urine uric acid test of 700 mg/dL
- Undersecreter
88
Prognosis/Referral:
| -what should you educate the Pt on regarding acute gouty attacks?
- 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
Describe Pseudogout
-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
Chondrocalcinosis=
Radiographic evidence of calcification in articular cartilage
91
Risk factors for Pseudogout
- 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
Most CPPD (aka pseudogout) is _____
idiopathic
| --but Early-onset familial CPPD with chromosomal linkages
93
Describe the pathophysiology of CPPD
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
Clinical Sx of CPPD (2 types)
- asymptomatic
| - Acute arthritis/pseudogout
95
Asymptomatic CPPD Pt lab findings
May see CPP deposition in a joint on a radiograph but have no symptoms
96
Acute Arthritis/pseudogout Sx
- 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
Chronic CPP crystal inflammatory arthritis (“pseudo-RA”) - describe this disorder
-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
OA with CPPD (“pseudo-OA”)
| Describe this disorder
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
Pseudo-neuropathic joint disease
=Severe joint degeneration from CPP crystal deposition
- Resembles neuropathic arthropathy
- Unlike neuropathic arthropathy, there is not usually any neurologic impairment
100
DDx for Acute arthritis/pseudogout
Gout
Septic arthritis
Trauma
Lyme disease
101
DDx for Chronic CPP
Osteoarthritis
Rheumatoid Arthritis
Peripheral spondyloarthritis
Neuropathic arthropathy
102
Dx: Lab findings for CPPD
* *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
Tx Acute pseudogout
- Aspiration then intraarticular glucocorticoid injection-->Triamcinolone
- NSAIDs: Indomethacin, naproxen, salicylates
- Colchicine
- Systemic corticosteroids (oral, IV, or IM)
104
Tx OA with CPPD
Treat like OA
105
Tx Pseudo-neuropathic joint disease
treat like charcot arthropathy
106
When should you consider Prophylaxis tx for CPPD?
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
Pseudo-RA prophylaxis:
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
Prognosis/Referral: CPPD
Attacks will resolve even without treatment
Can cause chronic symptoms
Can refer to rheumatology
109
Compare & contrast Gout and CPPD Arthropathy
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
