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Acute Care Seminar 1 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Hyperuricemia Causes

A

-Impaired renal excretion of uric acid is the dominant cause of hyperuricemia.
-Reduced Impaired ability to excrete uric acid accounts for 90% of cases

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2
Q

Secondary Hyperuricemia

A

-Caused by increased purine biosynthesis and/or urate production.

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3
Q

Clinical Diseases causing secondary hyperuricemia

A

-Renal disease
-Chronic acidosis - cyanotic heart disease
-Inherited Purine enzyme defects
-In most overproducers the defect remains obscure
-Hematologic disorders

-Drug Diet or Toxin induced
Ethanol (beer and spirits)
Fructose
Vitamin B 12 deficiency
Excessive intake of foods with purines
Drugs - thiazide, furosemide, cyclosporine

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4
Q

Labs

A

-Uric acid level, CRP, Creatinine, AST.

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5
Q

Serum Uric Acid Level

A

The presence of hyperuricemia supports but does not confirm a diagnosis of gout. (Note: during acute flare uric acid may be LOW due to crystallization in affected joints).

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6
Q

Serum Urate Levels

A

-in men increasing during puberty dramatically and remain at level that will be maintained in adulthood.
-Women do not reach maximum serum urate levels until after menopause (estrogen is protective).

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7
Q

PEARL

A

Patients with acute gout may have a normal serum uric acid during an attack

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8
Q

Diagnostic Testing of Gout

A

-Hyperuricemia supports, but does not confirm a diagnosis of gout.
-Joint aspiration should be considered at least once to confirm the presence of urate crystals if not contraindicated.
-A dual energy CT scan can detect the presence of uric acid deposits even after an acute flare

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9
Q

Gout

A

-Rapid onset of warmth swelling redness and pain in the affected joint

-Commonly seen in the great toes (i.e. podagra), but can affect other joints.

-Symptoms of crystal deposition include acute episodes of inflamed joints, chronic destruction of joint resulting in chronic gouty arthropathy and soft tissue manifestations such as tophi.

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10
Q

Cause of Gout

A

accumulation of monosodium urate crystals in around the tissues of joints.

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11
Q

4 stages of Gout

A

-asymptomatic hyperuricemia
-acute intermittent gout
-intercritical gout
-chronic tophaceous gout typical occurring after 10 years or more of acute attacks.
-Incidence rises w/ age and levels of hyperuricemia

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12
Q

Xrays of Gout

A

-Early findings include soft tissue swelling

-Later findings include asymmetric bony erosions slightly removed from the joint with appearance of an overhanging edge without joint space narrowing until very late in the disease.

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13
Q

Treatment Plan for Gout

A
  • Acute flare treatment

-Chronic uric acid lowering treatment
Gout flare prophylaxis for the starting treatment
Lab monitoring for those starting chronic uric acid lowering treatment
Uric acid every month until serum uric acid goal met
CBC, Creatinine, AST at 1 month and then every 6-12 months.
Lifestyle changes

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14
Q

Acute Gout Flare Treatment

A

-NSAIDS
-Colchicine 1.2 mg ORALLY at onset of a flare, followed by 0.6mg at 1h later if needed next day 0.6mg ORALLY once or twice daily; MAXIMUM of 1.2mg daily until flare is over.
-Oral Prednisone burst with rapid taper (such as 30mg prednisone daily for 3 to 5days).
-ICE

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15
Q

When to start chronic tx of gout

A

-Greater than 2 flares per year
-Any Tophi present
-Any destructive gout changes seen on x-ray
-Do not have to wait for flare to subside can start uric acid lowering agent right away
-Can consider starting uric acid lowering agent with only one gout flare (CKD >stage III, serum uric acid level >9, hx of kidney stones)

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16
Q

Hyperuricemia

A

Hyperuricemia is a predisposing factor for gout but doesn’t mean you will get gout

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17
Q

Uric Acid Lowering Medication

A

-Allopurinol start 100 mg a day, slowly titrated to achieve a goal uric acid of less than 6 mg/dL. (SJS for those with HLA-B*58:01 polymorphisms)
-Uloric used most often if allopurinol is not tolerated or effective. 40mg ORALLY once daily; dose may be increased to 80mg if uric acid goal is not met. -Black box warning

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18
Q

PEARL on stopping uric acid lowering agent

A

can cause an acute attack or worsen one.

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19
Q

Black box warning for Uloric

A

Cardiovascular thromboembolic events (cardiovascular deaths, non-fatal myocardial infarctions (MI), and non-fatal strokes) have been reported; monitoring insure decision making recommended

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20
Q

Prophylaxis treatment for gout

A

-Colchicine low dose 0.6 mg once to BID
-NSAIDS Naproxen 250 mg BID
-Prednisone less then 10 mg
-3 to 6 months (Three months beyond achieving uric acid goal)
-6 months beyond tophus resolution

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21
Q

Lifestyle changes for Gout

A

-Weight loss
-Diets low in purine
-Limit alcohol
-HFCS

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22
Q

Asymptomatic Hyperuricemia

A

-Recommendation is not to start treatment with uric acid lowering agent
-Even if there is crystal deposition seen on dual energy CT scan if patient has not had a gout flare.

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23
Q

Pseudogout

A

-acute inflammatory arthritisassociated withthepresence of calcium pyrophosphate dihydrate (CPPD) crystals in the joint space often self limited.
-Caused by inflammatory reaction to the CPPD crystals that release cytokines and other inflammatory mediators, resulting in intense inflammation of the affected joint.
-More often large joints. Attack can last longer than gout
-Knee most common then wrist, ankle and elbow.

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24
Q

Pseudogout Diagnosis

A

-Joint aspiration: Synovial fluid is typically inflammatory (>2,000 white cells)
-Calcium pyrophosphate dihydrate (CPPD) crystals are seen.
-Plain radiographs may show chondrocalcinosis, which is supportive of pseudogout but does not confirm the diagnosis.
-A metabolic cause should be considered (eg, hyperparathyroidism, hemochromatosis, hypothyroidism, hypomagnesemia) for patients with pseudogout

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25
Q

Aspiration of pseudogout

A

-Pseudogout is diagnosed by joint aspiration, as in gout.
-Under polarized microscopy, you see rhomboid crystals that are weakly birefringent, positively.
-They appear blue parallel to the direction of the compensator

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26
Q

PseudoGout Treatment

A

-The principles for treating pseudogout and gout are similar. NSAIDS, Colchicine & prednisone
-Untreated pseudogout is typically self-limited and usually resolves within 2 weeks.
-If aspiration is done, some symptoms may be relieved because the calcium pyrophosphate dihydrate crystals are removed.
-Most cases require treatment to alleviate pain.

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27
Q

4 types of inflammatory arthridities

A

-Rheumatoid Arthritis
-Ankylosing Spondylarthritis
-Psoriatic Arthritis
-Infectious Arthritis

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28
Q

Rheumatoid Arthritis

A

-Symmetric involvement, erosive deformities.
-Peripheral joints initially but can involve larger joints.
Spares spine (though can involve C1, C2) and DIP joints.
-Rheumatoid nodules, rheumatoid lung.
-Genetic predisposition,
Smoking, Unknown

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29
Q

Ankylosing Spondylarthritis

A

-Axial symptoms, Sacroiliitis
-Any region of spine, sacroiliac joint. Rare hips
-Uveitis, enthesitis
-Carriers of HLA-B27 gene.

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30
Q

Psoriatic Arthritis

A

-Axial symptoms, peripheral symptoms (typically asymmetric)
-Any region of spine, hand and feet (can involve DIP), wrist, ankle, sacroiliac joint
-Psoriatic skin lesions, nail involvement, iritis, enthesitis.
-Psoriasis. Family history.

31
Q

Infectious Arthritis

A

-Large joint > peripheral joints. (typically asymmetric, oligoarticular)
-Knee, ankle, SI joint
-Iritis, urethritis, dactylitis, enthesitis
-Approved list of pathogens: Chlamydia trachomatis, Yersinia, Salmonella, Shigella, Campylobacter, Escherichia coli, Clostridium difficile, and Chlamydia pneumoniae.

32
Q

Inflammatory Arthritides: Dx workup

A

-CBC, inflammatory markers (Erythrocyte sedimentation rate, C-reactive protein), CCP, Rheumatoid factor, HLA B27, and infectious work-up if there is concern for reactive arthritis. Other tests as pertinent based on history.)
-Ultrasound: Equipment and skill improving, can use in patients who are not able to undergo MRI.
-Xrays: Cornerstone to radiologic diagnosis they defined character and distribution of bone erosions, alignment issues
-MRI or bone scan: Helps to detail synovial proliferation for soft tissue evaluation.

33
Q

Synovial Fluid Analysis of inflammatory arthritides dx workup

A

Normal: Clear, viscous, pale yellow, 0-200 wbc, <10% PMNs
-Group 1: clear to slightly turbid, 200-2000 WBC, <20% PMNs, conditions-OA, Trauma, mechanical derangement, AVN
-Group 2: Slightly turbid, 2000-50,000 WBC, 20-70% PMNs, RA, Gout, PsA, Reactive arthritis, PMR, Infectious arthritis
-Group 3: Turbid to very turbid, >50,000 wbc, >70% PMNs, Sepsis, gout, reactive arthritis

34
Q

RA management

A

Short term: Prednisone (<20mg), Nsaids, Cortisone Injections

Longterm (initiated by specialist): DMARDs, Biologics

-DMARDS-methotrexate, sulfasalazine, hydroxychloroquine, leflunomide

35
Q

Ank Spon Tx

A

Short term: NSAIDs, Cortisone Injections

Long term: Biologics

36
Q

PsA Tx

A

Short term: NSAIDs, Cortisone Injections

Long term: DMARDs, Biologics

37
Q

Infectious/Reactive tx

A

Short term: Treat infectious etiology, NSAIDs, Prednisone (<20mg)

Long term: Rarely require additional tx

38
Q

OTC Options for inflammatory arthritides

A

topical therapies, diclofenac sodium gel, acetaminophen ER, NSAIDs

39
Q

Rheumatologic therapies

A

DMARDS:
Hydroxychloroquine
Sulfasalazine
Methotrexate
leflunomide
Azathioprine
Mycophenolate mofetil

S/E:
-Minor (Nausea, stomatitis, headache, fatigue)
-Serious but rare (Pancytopenia, Liver fibrosis (NASH), Hypersensitivity pneumonitis)
-Note: take several weeks to months to reach efficacy.

40
Q

Biologics

A

-Immune Cell Mediated
Cytokines
-TNF Alpha Inhibitors (ex: humira, enbrel)
-IL-1, IL-6, IL-6 Receptor, JAK inhibitor
Lymphocyte
-Bcells, BAFF etc.

S/E: are rare but serious - (Neurologic, Cancer risk, GI perforation)
Serious Infection risk is real

41
Q

Info on RA meds

A

-Many medications require laboratory monitoring
-Increased infection risk present with most therapies.
-Keep in mind some DMARDs noted to have drug-drug interaction with several antibiotics.
-When to hold therapies
Infections and treatment for infection
Medication interactions
Surgeries (more information later slide)

42
Q

Hospital Presentations: Presenting w/ new rheumatic disease process

A

-Acute monoarticular joint process
-FUO
-Can present with more systemic symptoms dependent on disease (Hemolytic anemia, pericarditis, rash organ failure)

43
Q

Hospital Presentations: Presenting w/ established rheumatic disease process

A

Flare
Infections
Joint replacement
Progressive disease
Medication reactions

44
Q

Acute Monoarthrtits

A

Hx: Any history of trauma, cancer, or acute on chronic arthropathy?
Critical Tests for early dx;
-Synovial fluid analysis
-xray
-infectious eval as applicable
-Gram stain: Gram positive organisms is 80% of cases

45
Q

Acute Monoarthritis: Septic Arthritis

A

-Bacteremia (Skin infections)
-Immunocompromised host
(Rheumatoid arthritis, diabetes, alcoholism, older age)
-Poverty, IV drug use
-Surgical procedures
-Sexual activity

46
Q

Routes by which bacteria reach the joint

A

-Hematogenous route
-Dissemination from osteomyelitis
-Spread from an adjacent soft tissue infection
-Diagnostic or therapeutic measures
-Penetrating damage by puncture or trauma

47
Q

Acute Nongonococcal Bacterial Arthritis

A

-Clinical manifestations
80% are monoarticular
Knee > hip > others
-An erythematous, warm, very tender joint
-Less impressive if immunocompromised
-Fever
-Staphylococcal aureus is the most common organism

48
Q

Acute Nongonococcal Bacterial Arthritis Tx

A

-Joint aspiration sent for cell count, crystals, culture/sensitivities
-Orthopedics consult -arthroscopic lavage
-IV antibiotics (make appropriate alterations based on culture/sens results)
-Pain management

49
Q

Acute Gonococcal Bacterial Arthritis Clinical Manifestations

A

-Migratory arthralgias
-Tenosynovitis
-Maculopapulovesicular, petechial and necrotic skin lesions on the feet
-Fever in only 50%
-Polyarticular involvement in 50%

50
Q

Acute Gonococcal Bacterial Arthritis: Dx tests

A

-Culture joint, blood, urogenital, rectal and pharyngeal mucosa
-HIV, syphilis serologies
-Total hemolytic complement in recurrent cases of disseminated neisserial infections
-Check for concomitant Chlamydia infection

51
Q

Acute Gonococcal Bacterial Arthritis: Tx

A

-IV Ceftriaxone 1-2 grams daily for 7 days, then switch to amoxicillin for another 1-2 weeks
-Treat all sex partners with ceftrioxone 250 mg IM and azithromycin 1g orally.
-Arthroscopic lavage is not needed in most cases unless a delay in diagnosis

52
Q

Osteoarthritis

A

osteoarthritis results from a complex interplay of multiple factors, including joint integrity, genetic predisposition, local inflammation, mechanical forces, and cellular and biochemical processes
Incidence: As above, high prevalence in in-patient setting.

53
Q

OA Symptoms: Predisposing factors: age, trauma, genetics

A

Less common in people younger than 40 years old but rate increase with age. Typically presents in the fifth and sixth decades.
Affects adult men more than women until after age 55.
Pain and stiffness in one or more load bearing joints are the initial symptoms.
Hallmark symptoms include pain and stiffness aggravated by weightbearing, tenderness, and swelling. Symptoms are alleviated by resting the joint.
Presents insidiously, asymptomatic articular surface changes are common in the fourth decade.
Stiffness usually resolves within 30 minutes of joint use.

54
Q

OA Physical Exam

A

Most commonly focused on central joints.
Bony enlargement and cool joint effusion.
Later findings can include joint deformities
(osteophytes including Heberden and Bouchard nodes), muscle wasting, and gait disturbance.

55
Q

OA Dx

A

Use of x-ray
Synovial fluid analysis (pseudogout common)
MRI
CT, bone scan, and ultrasound have less utility.

56
Q

OA management

A

Pharmacologic therapy
NSAIDs
Injections (steroid, Synvisc)

Nonpharmacologic therapy
Weight loss, Physical therapy

Surgical options
Joint replacement to appropriate joints

When to refer
Consideration should be made for able patient to complete physical therapy
Failure of conservative measures consider referral to orthopedics

Implications for the hospitalized patient
Consider pseudogout

57
Q

Connective Tissue Diseases

A

-Sjorgren’s
-Systemic Lupus erythematosus
-Scleroderma
-Diseases often evolves slowly over time. Symptom onset to diagnosis is approximately 9 months in lupus
-Currently no diagnostic criteria – diagnosis is made based on individuals’ constellation of symptoms, laboratory findings, and additional testing.

58
Q

Sjorgen’s

A

-Sicca symptoms (dry eye, dry mouth, dry skin), parotitis, rash, inflammatory arthritis
-Initial tx: Symptomatic, dependent on organ system involved.

59
Q

Systemic Lupus

A

-Fevers, fatigue, oral ulcers, inflammatory arthritis, Raynauds, rash, photosensitivity, pleurisy, renal involvement
-Butterfly rash, red patches, mouth and nose ulcers
-Effects multiple organs: Heart, lungs, skin, blood, muscle and joints
-Initial Tx: Prednisone as induction for most organ systems involved.

60
Q

Scleroderma

A

-Severe Raynauds, sclerodactyly, puffy hands, dysphagia, reflux, lung disease, inflammatory arthritis
-Initial Tx: Dependent on organ system involved.

61
Q

ANA testing

A

Medications/Diagnoses causing ANA positivity
-Hypothyroidism, Rheumatoid, Multiple sclerosis, any connective tissue disease
-Drug induced: Procainamide, Hydralazine, Quinidine, Isoniazid, Minocycline (5/10000 pts), Anti-TNF, Methyldopa
-ANA testing for connective tissue disorders

62
Q

Hyperuricemia associated with what diseases

A

-CKD, CVD, HTN, insulin resistance syndrome.

63
Q

Curing GOUT

A

-Gout flares more common in first year b/c it’s getting out of the joint. If continuing gout lowering agent consistently the flares will subside altogether
-Once you’re 18 months out and consistent with medications it is almost cured

64
Q

Preventing tophaceous gout & chronic joint destruction

A

-If history of gout or found to have allopurinol in their past ask why patient is not on treatment now

65
Q

Connective Tissues Diseases: Management Pharm

A

-Prednisone
-Antimalarials (ie. hyroxychloroquine)
-DMARDS
-Plasmapheresis (hospital)
-Specific disease manifestations
—–raynauds-CCB
—–Sicca Symptoms-conservative measures

66
Q

Connective Tissue Diseases management non-pharm

A

-BP management
-Statins for LDL >100 mg/dl
-Tobacco cessation counseling
-Pregnancy counseling for active SLE and nephritis
-UV light protection
-Vaccinations
-management of fatigue and cognitive problems a challenge

67
Q

Myositis

A

-Disorders which cause nonsuppurative muscle inflammation

68
Q

Vasculitis

A

-Inflammation in the blood vessels.
-It causes changes in the walls of blood vessels, including thickening, weakening, narrowing and scarring.
-There are many types of vasculitis, and most of them are rare.
Vasculitis can effect one organ such as your skin, or it can be systemic. The condition can be acute or chronic.

69
Q

Medium Vessel Vasculitis

A

PolyarteritisNodosa Kawasaki Disease

70
Q

Large Vessel Vasculitis

A

Giant Cell Arteritis
Takayasu Arteritis

71
Q

Small Vessel Vasculitis

A

ANCA Associated GPA MPA EGPA

72
Q

Immune Complex Vasculitis

A

Cryoglobulnemic IgA (HSP) Hypocomplemen-temic Urticarial Vasculitis

73
Q

Giant Cell (Temporal) Arteritis

A

-Inflammation of the large and middle-sized blood vessels more likely found in cranial arteries also called Temporal Arteritis
-HA: Pain at temples
-Scalp tenderness
-Signs ischemic optic neuropathy
-Jaw claudication- pain while chewing
-Arm claudication - muscle cramping with use, color changes
-Pulselessness or diminished pulses
-asymmetric BPs (suggest large vessel involvement)
-Clinical abnormal temporal artery-femoral or abdominal bruits, asymmetric radial or pedal pulses, carotid or subclavian bruits

Acute Care Seminar 1 (31 decks)

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