rheum III and IV Flashcards

1
Q

gout

A
  • deposition of uric acid crystals in joints, tissues, fluids
  • hyperuricemia does NOT equal gout
  • common with other comorbidities
  • extremely painful
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

tophi

A
  • uric acid crystals in tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the cause of 90% of gout cases?

A
  • under excretion

- mostly associated with renal disorders

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

over production of uric acid is mainly associated with what?

A
  • excessive dietary purines like red meat, organ meat, shellfish
  • beer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

risk factors for gout

A
  • male
  • advanced age
  • AA or pacific islander
  • alcohol and high purine intake
  • obesity, HTN, hyperlipidemia, diabetes
  • diuretics (HCTZ)
  • lead exposure
  • women after menopause
  • genetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

clinical presentation of gout

A
  • podagra
  • very tender
  • acute onset
  • redness
  • 50% first attack in MTP of great toe
  • predilection for feet, ankles, toes
  • renal sx- uric acid stones and gouty nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

PE findings with acute gout

A
  • usually monoarticular and TTP

- skin is warm, tense, red

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

PE findings with chronic gout

A
  • tophi deposition
  • CT destruction and gross deformities
  • infection
  • drainage
  • bone destruction and erosion -> functional loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

differential dx for gout

A
  • cellulitis
  • bug bite
  • septic joint
  • RA
  • pseudogout
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

diagnosis of gout

A
  • arthrocentesis shows intracellular UA crystals*
  • negative birefringence under microscopy*
  • check gram stain
  • elevated UA > 6.8 (not diagnostic)
  • get 24 hour urine
  • xrays
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

xray findings in gout

A
  • early on only soft tissue swelling

- late shows bony erosions with sclerotic margins, calcification

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

acute gout treatment

A
  • diet modifications
  • NSAIDs first line (indomethacin) within 24 hrs
  • 2nd line- colchicine
  • 3rd line- steroids
  • antihyperuricemic tx for prevention and reversal of consequences
  • treat comorbidities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

chronic gout treatment

A
  • lower urate level to < 5
  • 2-4 weeks after acute attack f/u and check urate levels
  • allopurinol first line
  • probenecid is first line if allopurinol is c/i
  • colchicine for flares
  • NSAIDs
  • cherries decrease gout risk
  • combo drugs if levels not achieved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

indications for chronic gout treatment

A
  • multiple attacks
  • tophaceous deposits
  • gout with renal insufficiency
  • nephrolithiasis even after tx
  • uric acid levels of 6.5 +
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

pseudogout

A
  • chondrocalcinosis
  • Ca pyrophosphate dihydrate (CPPD) deposition
  • mainly affects knees
  • can be asymptomatic or mimic other diseases
  • often occurs following anesthesia/ surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

risk factors for pseduogout

A
  • hypercalcemia

- metabolic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

clinical presentation of pseudogout

A
  • may be asymptomatic
  • monoarticular
  • often in knee
  • can affect wrists, MCP, hips, shoulders, elbows, ankles
  • red, warm, tender, swollen
  • valgus deformity
  • often resolves on its own
  • fever possible
  • ligamentum flavum in spine involved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

diagnosis of pseudogout

A
  • CPPD deposition in kidneys and joints
  • CPPD stone
  • positive birefringence rhomboid crystals*
  • elevated ESR and CRP
  • chondrocalcinosis on xrays**
  • test for serum Ca, P, Mg, Alk phos, TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

differential dx of pseudogout

A
  • gout
  • septic arthritis
  • RA if polyarticular
  • primary or post-traumatic OA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

acute treatment of pseudogout

A
  • NSAIDs
  • colchicine short term
  • steroids short term
  • drain fluid
  • rest/ice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

chronic treatment of pseudogout

A
  • > 3 attacks per year
  • 1st line- colchicine
  • 2nd line- NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Fibromyalgia

A
  • chronic pain disorder wit widespread pain and allodynia
  • central sensitization
  • usually women 20-50
  • increased incidence of depression, anxiety, HA, IBS, chronic fatigue syndrome, SLE, RA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

allodynia

A
  • pain d/t stimulus that does not normally provoke pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

clinical manifestations of fibromyalgia

A
  • widespread pain
  • abnormal tenderness, fatigue, sleep disturbances, autonomic disturbances
  • GI or GU sx
  • chronic HA, poor concentration, memory disorder
  • stiffness
  • sensation of swelling without evidence of swelling**
  • widespread multiple tender points**
  • paresthesias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

when are fibromyalgia sx worse

A
  • in AM
  • before bed
  • cold
  • stress
  • new exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

diagnosis of fibromyalgia

A
  • dx of exclusion**
  • generalized body pain for at least 3 mo
  • at least 11 of 18 specific tender points
  • check CBC, vit D, TSH
  • sleep study
  • imaging- brain MRI
  • xray to r/o OA or DJD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

treatment for fibromyalgia

A
  • CBT
  • exercise
  • weight reduction and nutrition counseling
  • acupuncture, massage, chiro
  • 1st line- tylenol or tramadol ; tylenol/tramadol (ultracet)
  • 2nd line- TCAs
  • 3rd line- SSRI, milnacipram, pregabalin, gabapentin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Raynaud’s phenomenon

A
  • abrupt onset of well demarcated pallor of digits -> cyanosis with pain and numbness -> reactive hyperemia
  • vasospastic phenomenon
  • precipitated by cold or stress
  • associated with CREST syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

CREST syndrome

A
  • calcinosis
  • Raynaud’s
  • esophageal dysmotility
  • sclerodactyly
  • telangiectasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

clinical manifestations

A
  • vasospastic attack usually only in fingers
  • vasospasm can occur in toes, nose, ears, lips
  • PE is normal between attacks in primary cause
  • in secondary cause pits or ulcerations on finger tips may be present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

diagnosis of raynaud’s

A
  • history
  • primary- attacks precipitated by cold and bilat without gangrene
  • for secondary need to r/o other systemic illnesses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

treatment of raynaud’s

A
  • best pharm tx= Ca channel blockers** (amlodipine and nifedipine)
  • mittens for cold
  • avoid nicotine d/t potent vasoconstriction
  • beta blockers may exaggerate sx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

SLE

A
  • chronic autoimmune inflammatory disease
  • can attack any body sys at any time
  • relapse and remitting
  • severity of disease varies
  • cause unknown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

epidemiology of SLE

A
  • majority are women of child bearing age
  • AA, latinos, and asian women at higher risk
  • familial occurence
  • when men affected they have a higher 1 year mortality rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

triad of SLE

A
  • fever
  • arthralgia/ arthritis
  • butterfly rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

common symptom clusters of SLE

A
  • cutaneous, articular and renal sx

- CNS, thrombotic, and muscular sx

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

acute cutaneous lupus erythematosus

A
  • photosensitive rash- malar rash, maculopapular rash on dorsum of hands, or bullous
  • non-scarring alopecia that correlates with disease activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

subactue cutaneous lupus erythematosus

A
  • papulosquamous or annular scaly rash (psoriaform)
  • most photosensitive
  • torso and limb, spares face
  • have anti-SSA and anti-SSB ab
  • often induced by HCTZ or terbinafine
  • half of these pts dev SLE
39
Q

chronic cutaneous lupus erythematosis

A
  • discoid lupus
  • lupus panniculitis
  • chilblain lupus
40
Q

discoid lupus

A
  • coin shaped
  • raised erythematous plaque with scale
  • face, scalp, ears, neck
  • can scar and lead to skin atrophy
  • mainly disease of skin and often doesn’t go on to SLE
41
Q

lupus panniculitis

A
  • deep nodules

- scalp, face, arms, buttocks, thighs

42
Q

chilblain lupus

A
  • resembles frost bite
43
Q

nonspecific skin lesions associated with lupus

A
  • vasculitis, purpura, livedo reticularis
  • raynaud’s
  • non-scarring alopecia
  • nail fold telangiectasias
  • bullous lesions
44
Q

diagnostic criteria for SLE

A
  • need four of “SOAP BRAIN MD” to dx, can occur at different times
  • serositis
  • oral ulcers
  • arthritis, nonerosive
  • photosensitivity
  • blood/heme disorders
  • renal disorders
  • ANA
  • immunologic disorders
  • neurologic disorders
  • malar
  • discoid
45
Q

oral ulcers of SLE

A
  • painless
  • can occur anywhere in mouth
  • ulcerations, erythema or petechiae
  • can also appear in nose, usually nasal septum
46
Q

arthritis of SLE

A
  • symmetrical
  • non-erosive
  • pain, swelling, joint effusion
  • deformities secondary to loosening of ligaments- Jaccoud’s arthritis
  • also causes myalgia, myositis, tenosynovitis, tendonitis, AVN
47
Q

pleuritis and SLE

A
  • tissue around lungs becomes inflamed
  • painful breathing and chest pain
  • pleural effusion and interstitial lung disease also possible
48
Q

heart involvement and SLE

A
  • often pericarditis
  • increased risk MI and arrhythmias
  • myocarditis
  • endocarditis- libman sack
  • accelerated atherosclerosis
49
Q

renal disorder of SLE dx

A
  • best= biopsy
  • persistent proteinuria > 0.5 g/day or 3+ on dipstick
  • cellular casts in urine
50
Q

renal disorder and SLE

A
  • most frequent cause of disease related death
  • worse prognosis if SCr > 2.4 mg/dL
  • usually asymptomatic
  • gross hematuria, glomerulonephritis, nephrotic syndrome, acute or end stage RF, HTN
51
Q

most common neurologic disorders associated with SLE

A
  • seizures
  • psychosis
  • must rule out other offending agents first
52
Q

hematologic disorders of SLE

A
  • hemolytic anemia with reticulocytosis
  • leukopenia on 2+ occasions
  • lymphopenia on 2+ occasions
  • thrombocytopenia
  • 50% of pts will have leukopenia that correlates with disease activity
53
Q

ANA testing in SLE

A
  • 98% have positive ANA
  • ANA does NOT equal SLE
  • if positive get titer, pattern, and extractable nuclear antigens (ENA)
54
Q

ANA titer

A
  • estimate of how many ANA present
  • high titer= more severe disease
  • lowest dilutent is 1:40
  • highest dilutent is 1:2560, very severe disease
55
Q

ANA pattern

A
  • suggests presence of SLE subtypes
56
Q

diffuse/ homogenous ANA pattern

A
  • associated with drug induced lupus
57
Q

rim/peripheral ANA pattern

A
  • most specific for SLE
58
Q

speckled ANA pattern

A
  • assoc with SLE and other diseases

- not specific to SLE

59
Q

nuclear/ centromere ANA pattern

A
  • associated with scleroderma
60
Q

ENA’s associated with SLE

A
  • anti-dsDNA (correlates to disease activity)

- anti-SM- specific to SLE but not sensitive

61
Q

antiphospholipid antibodies (APLs) in SLE

A
  • associated with high risk blood clot and miscarriages
  • abnormal IgG or IgM
  • pos test for lupus anticoagulent if pt has had miscarriage or prolonged PTT
  • often have false pos for syphilis
62
Q

complement proteins in SLE

A
  • usually low during disease activity
63
Q

treatment for SLE

A
  • refer to rheum***
  • NSAIDs for joint pain, pleuritis but avoid sulfa based
  • steroids for flares
  • hydroxychloroquine for joint pain, fatigue, derm but risk of retinopathy - VFT every year
  • immunosuppressants (non-biologics first then biologics)
  • topical steroids for skin
  • anticoags for pts with antiphospholipid syndrome
64
Q

lupus and pregnancy

A
  • 20X higher rate miscarriage
  • considered high risk pregnancies
  • disease flares in 3rd trimester or post-natal pd
  • antiphospholipid syndrome -> early pregnancy loss
  • all pregnant women screened for anti-SSA and anti-SSB because can cause neonatal lupus (complete heart block)
65
Q

drug induced lupus

A
  • fever, arthralgia, myalgia, pleuritis, pericarditis, neurologic sx, and other features of SLE
  • no renal involvement
  • pos ANA but no SLE Ab
  • anti-histone Ab
  • treat by d/c offending drug, give NSAIDs and steroids
66
Q

drugs that commonly cause drug induced lupus

A
  • methyldopa
  • procainamide
  • hydralazine
  • isoniazid
  • chlorpromazine
  • TNF blockers
  • quinidine
  • carbamazepine
  • minocycline
  • phenytoin
67
Q

localized scleroderma types

A
  • morphea

- linear

68
Q

morphea scleroderma

A
  • common in kids
  • single or multiple patches of hard skin on trunk
  • often spontaneously disappears
69
Q

linear scleroderma

A
  • linear bands of hard skin across face, arms, legs
  • may involve muscle or bone
  • en coup de sabre- linear patch on scalp/ face
70
Q

systemic sclerosis

A
  • aka scleroderma
  • multisystem autoimmune disease
  • diffuse fibrosis of skin and internal organs
  • overproduction of collagen
  • classified as either diffuse or limited cutaneous scleroderma
71
Q

what is CREST syndrome

A
  • limited cutaneous scleroderma
  • calcinosis
  • Raynaud’s
  • esophageal dysmotility
  • sclerodactyly
  • telangiectasias
  • 80% of pts with scleroderma have CREST
72
Q

cause of scleroderma

A
  • unknown
  • likely genetic and environmental factors
  • coal miners and stone masons at higher risk d/t silica dust
73
Q

pathogenesis of scleroderma

A
  • vascular fibroproliferative changes in arteries and arterioles
  • excessive and progressive collagen deposition in skin and internal organs
  • immunologic changes
74
Q

clinical manifestations of CREST

A
  • restricted and slow progression of skin and distal extremities
  • chronic raynaud’s
  • nailfold dilated capillaries
  • late incidence of pulmonary HTN
  • good prognosis
75
Q

clinical manifestations of diffuse cutaneous scleroderma

A
  • widespread and rapidly progressive skin thickening of trunk, distal and prox extremities
  • Raynaud’s after one year of skin changes
  • hypo/ hyperpigmentation
  • nailfold dilated capillaries
  • early involvement of lungs, heart, GIT, kidneys
  • muscle and tendon inflammation -> tendon friction rub
  • poor prognosis
76
Q

antibodies associated with CREST

A
  • anti-centromere Ab
77
Q

antibodies associated with diffuse cutaneous scleroderma

A
  • anti-SCL- 70 (anti-topoisomerase I)- indicates poor prognosis and assoc with lung disease
  • anti-RNA I/ III polymerase Ab- associated with rapidly progressive diffuse skin, renal, and cardiac disease, poor prognosis
78
Q

stages of sclerodactyly

A
    1. edematous stage- “puffiness”, shiney without folds
    1. inflammatory- thickening destroys normal oil and sweat glands -> dry skin with intense itching
    1. atrophic stage- skin is tight and waxy, dev joint contractures
79
Q

diagnosis of scleroderma

A
  • requires one major or 2+ minor sx
  • other sx help support dx
  • often have pos ANA with nucleolar pattern
  • anti-SCL-70, anti-centromere, or anti-RNA polymerase may be seen
80
Q

major sx of scleroderma

A
  • proximal scleroderma
81
Q

minor sx of scleroderma

A
  • sclerodactyly
  • digital ischemia with pitting scars or atrophy of finger pads
  • bibasilar pulmonary fibrosis
82
Q

treatment for scleroderma

A
  • no disease modifying meds
  • refer to rheum**
  • prob will require other specialists
  • treat symptomatically
83
Q

prognosis of scleroderma

A
  • worse in diffuse
  • worse in blacks, males, older pts
  • risk of lung and esophageal cancers
84
Q

what is the most common cause of death in scleroderma

A
  • lung disease (ILD or pulm HTN)

- cardiac and kidney disease death also common

85
Q

Sjogren’s syndrome

A
  • chronic systemic autoimmune disease
  • destroys exocrine glands
  • dry mouth and eyes
  • majority of pts are women in 50s
  • increased risk of non-hodgkins lymphoma**
86
Q

basic pathogenesis of sjogren’s

A
  • unknown trigger -> vascular endothelial cells in exocrine glands (in genetically predisposed pts)
  • lymphocytes activated
  • cytokines released
  • gland inflammation and destruction -> sicca sx and parotid swelling
87
Q

primary Sjogren’s

A
  • dry eye and mouth
88
Q

secondary Sjogren’s

A
  • complication of another autoimmune disease
89
Q

sx of Sjogren’s

A
  • dry eye*
  • dry mouth*
  • difficulty chewing/ swallowing
  • increased cavities
  • bilat parotitis
  • dry skin, nose, vagina
  • muscle/ joint pain and weakness
  • will likely have another autoimmune disease
90
Q

diagnostic criteria for Sjogren’s

A
  • need at least 2 of the following:
  • ocular staining score of at least 3 or more
  • biopsy of salivary glands shows lymphocytic sialadenitis
  • pos anti-SSA or anti-SSB
  • pos RF and ANA
91
Q

schrimers test

A
  • test for Sjogren’s
  • measures tear production
  • pos if < 5 mm of wetting after 5 min
92
Q

rose bengal staining

A
  • test for Sjogren’s
  • put solution in eye
  • slit lamp shows flecks of red over lower portion of cornea and conjunctiva
93
Q

labs for Sjogren’s

A
  • ANA
  • Anti SSA and SSB
  • complement levels- low in severe
  • cyroglobulins in severe
  • CBC with diff
  • thyroid Ab often present
  • ESR elevated out of proportion to CRP
94
Q

treatment of Sjogren’s

A
  • symptomatic
  • artificial tears
  • biotene products
  • fluid intake, gum
  • avoid anithistamines and anticholinergics
  • dentist, fluoride
  • muscarinics like cevimeline or pilocarpine