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
2
Q
tophi
A
- uric acid crystals in tissue
3
Q
what is the cause of 90% of gout cases?
A
- under excretion
- mostly associated with renal disorders
4
Q
over production of uric acid is mainly associated with what?
A
- excessive dietary purines like red meat, organ meat, shellfish
- beer
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
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
7
Q
PE findings with acute gout
A
- usually monoarticular and TTP
- skin is warm, tense, red
8
Q
PE findings with chronic gout
A
- tophi deposition
- CT destruction and gross deformities
- infection
- drainage
- bone destruction and erosion -> functional loss
9
Q
differential dx for gout
A
- cellulitis
- bug bite
- septic joint
- RA
- pseudogout
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
11
Q
xray findings in gout
A
- early on only soft tissue swelling
- late shows bony erosions with sclerotic margins, calcification
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
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
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 +
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
16
Q
risk factors for pseduogout
A
- hypercalcemia
- metabolic conditions
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
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
19
Q
differential dx of pseudogout
A
- gout
- septic arthritis
- RA if polyarticular
- primary or post-traumatic OA
20
Q
acute treatment of pseudogout
A
- NSAIDs
- colchicine short term
- steroids short term
- drain fluid
- rest/ice
21
Q
chronic treatment of pseudogout
A
- > 3 attacks per year
- 1st line- colchicine
- 2nd line- NSAIDs
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
23
Q
allodynia
A
- pain d/t stimulus that does not normally provoke pain
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
25
Q
when are fibromyalgia sx worse
A
- in AM
- before bed
- cold
- stress
- new exercise
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
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
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
29
Q
CREST syndrome
A
- calcinosis
- Raynaud’s
- esophageal dysmotility
- sclerodactyly
- telangiectasia
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
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
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
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
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
35
Q
triad of SLE
A
- fever
- arthralgia/ arthritis
- butterfly rash
36
Q
common symptom clusters of SLE
A
- cutaneous, articular and renal sx
- CNS, thrombotic, and muscular sx
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
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
- edematous stage- “puffiness”, shiney without folds
- inflammatory- thickening destroys normal oil and sweat glands -> dry skin with intense itching
- 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
