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Systemic Conditions Flashcards

1
Q

Ankylosing spondylitis

A

Chronic inflammatory disorder of axial skeleton resulting in formation of new bone at attachments of ligaments and tendons
Caucasian, male, 15-35 yrs, HLA-B27
DX: inflammatory back pain + x-ray (SI joint fusion, sacroiliitis, bamboo spine, etc)
+Schober’s, increased ESR, CRP, alk phos

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2
Q

CRPS

A

pain syndrome d/t nerve disorder that occurs at site of injury where patient experiences intense, burning pain in one or more extremities; results in pain that is usually non-anatomic and disproportionate to initial event or expected healing response

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3
Q

Describe/define OA

A

Progressive degeneration, loss of articular cartilage, subchondral bone and joint capsule of synovial joints. Pain from effusion (stretching joint capsule), increased vascular pressure on subchondral bone, periarticular myospasm or bursa inflammation, or torn meniscus or fibrocartilage complexes. Can be d/t wear and tear or secondary to metabolic disturbances, genetic predisposition etc.

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4
Q

Osteoporosis definition/description

A

General decrease in bone density resutls in fragile bones and increased risk of fractures, even after minimal trauma. Axial skeleton most affected, as well as pelvis and proximal long bones (femur).

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5
Q

Gout

A

Group of metabolic conditions that manifest in acute arthritic events initiated by urate crystals in affected joints and soft tissues
Acidosis predisposes to crystal formation
HTN, obesity, diabetes, hyperlipidemia, renal insuff, genetics, high purine diet, dehydration, starvation, hypothyroidism…etc
Spontaneous onset painful, hot, erythematous, tender, swollen MTP joint
Early x-ray unremarkable; later can show bony erosion, joint space narrowing and joint destruction
Labs: hyperuricemia
Dx: joint aspiration during attack shows monosodium urate crystals in synovial fluid

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6
Q

What pain med can pts w/ gout NOT have?

A

aspirin - can alter uric acid levels and prolong attack

Can use NSAIDs. Indomethacin, COX-2 inhibitors, Colchicine (w/in first 24 hrs), allopurinol are options.

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7
Q

What is the goal of gout tx?

A

Keep serum uric acid levels to 6mg/dL or less

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8
Q

What is the pathophysiology of OA?

A

Early: mechanical lesion or stress leads to degenration. Mild subchondral reactive sclerosis. Synovial fluid loses viscosity and cartilage wears out. Chondrocyte metabolism increases production of cartilage matrix destroying enzymes

Middle: Irregular joint space due to loss of cartilage, cartilage fragmentation (joint mice), reactive sclerosis.

Late: osteophytes, periarticular fibrosis, cartilage calcification, subchondral cysts (geodes). Exposure of subchondral bone after loss of cartilage causes joint instability, compensatory bone overgrowth and remodeling (reactive sclerosis and osteophyte formation). Fibrous adhesions and bony ankylosis may occur. Breakdown products create chronic inflammatory repsonse in synovium

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9
Q

Risk factors for OA

A

female (more likely to develop OA in hands)

age, obesity, trauma, genetics, menopause, infection, crystal deposition, acromegaly, previous RA

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10
Q

Presentation of OA

A

gradual onset of deep, achy joint pain worse in morning, better with mild activity and worse with excessive activity
limited ROM, crepitus
pain at rest or at night indicates severe progression
affected by changes in barometric pressure

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11
Q

OA PE

A

Heberden’s nodes (DIP)
joint enlargement
limited ROM
crepitus and pain w/ passive motion

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12
Q

Ortho tests for OA

A

anything that compresses damaged cartilage can reproduce symptoms (Scour, Ellman’s, etc)

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13
Q

X-ray findings in OA

A

large weight bearing joints: non-uniform joint space loss, subchondral sclerosis and cysts, osteophyte formation, joint mice

spine: osteophytes, facet arthrosis, loss of disc height, curve changes

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14
Q

What is the pathophysiology of OA?

A

exact mechanism not well understood
bone loss occurs without symptoms, fracture is often first indication of problem
typical preceding events are menopause, advanced age
bone mass peaks in mid 20’s
women lose a greater percentage of cortical bone and trabecular bone over lifetime compared to men

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15
Q

What are the types of OA?

A

postmenopausal - thought to result from estrogen and testosterone deficiency
senile - d/t decreased formation of bone and decreased renal production of vitamin D3 occuring later in life
secondary - d/t medications (glucocorticoids) or other conditions

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16
Q

Risk factors for OA

A 
female
age
genetics
European or Asian descent
Strenuous exercise resulting in amenorrhea
Smoking, alcohol, low physical activity
Low calcium, vitamin D intake
Parathyroid abnormalities
Low BMI
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17
Q

Presentation of OA

A

usually asymptomatic until fracture
gradual height loss, increased kyphosis
fracture may cause: severe back pain, loss of height, thoracic kyphosis, breathing difficulties if kyphosis and rib fractures, reduced mobility

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18
Q

Ddx for OA

A 
Cushing's syndrome
Intestinal malabsorption (calcium, vitamin D)
Hyperthyroidism 
Hyperparathyroidism
Immobilization (disuse osteoporosis)
glucocorticoid use
renal osteodystrophy
multiple myeloma or cancer metastasis
osteomalacia
Paget's disease
19
Q

OA Imaging

A

DEXA is gold standard (dual energy x-ray absorptiometry)
reported as T-scores which represent number of standard deviations from mean bone density values in healthy young adults
-1 to -2.5 SD is osteopenia
-2.5 is osteoporosis

Redo DEXA every 1-2 years

20
Q

Describe/define psoriatic arthritis

A

seronegative spondyloarthropathy usually associated with psoriasis - associated with human leukocyte antigen risk factors

autoimmune inflammatory reaction

21
Q

Risk factors for psoriatic arthritis

A

female = male
genetics, family history
can occur at almost any age

22
Q

Presentation of psoriatic arthritis

A

skin scales, red plaques
pitting of nails
asymmetrical oligoarticular arthritis (fewer than 5 joints)
digist of hands and feet affected first
dactylitis (sausage digits)
symmetrical polyarthritis - differentiate from RA by presence of DIP involvement, no subQ nodules, negative RF factor

23
Q

Ddx for psoriatic arthritis

A 
gout
OA
RA
reactive arthritis
septic arthritis
24
Q

Labs and imaging for psoriatic arthritis

A

Negative RF, ANA
Elevated ESR, CRP, mild anemia

X-ray:
Pencil in cup deformity
erosions, joint space narrowing
no ulnar deviation (as seen in RA)
soft tissue swelling
25
Define/describe reactive arthritis
seronegative polyarthropathy that follows infection and results in: conjunctivitis, urethritis, polyarthritis
26
Risk factors for reactive arthritis
male prior infection with chlamydia Caucasian descent
27
Presentation of reactive arthritis
Urethritis (male): dysuria, increased urgency, penile discharge, prostatitis (fever, chills, buring with urination, urgency) Urethritis (female): burning urination, inflammation of cervix or urethra, salpingitis, vulvovaginitis Conjunctivitis: crusty eyelids in morning or burning painful erythema with exudate, can increase in severity to iritis or uveitis Polyarthritis: painful, tender, swollen joints; usually asymmetric, predominantly lower limbs, 50% have low back/butt pain
28
PE of reactive arthritis
``` conjunctivitis keratoderma blennorragicum (rash on palms and soles of feet) thickening of finger or toenails lesions on penis oral ulcers acute uveitis aortitis (late finding, rare) mild renal pathology with proteinuria decreased lumbar flexion d/t pain ```
29
Ddx for reactive arthritis
``` ankylosing spondylitis gout/pseudogout psoriatic arthritis rheumatoid arthritis septic arthritis IBD ```
30
Imaging of reactive arthritis
x-ray: symptoms won't show up for several months, but wil show periosteal changes cortical erosions in early stages, fluffy periosteal changes as progresses non-marginal syndesmophytes esp. thoracolumbar spine sacroiliitis (usually unilateral)
31
Lab results in reactive arthritis
HLA-B27 common but not diagnostic anemia (normo, normo) elevated ESR, CRP, IgA usually RF, ANA are WNL Joint aspirate shows: inflammation (if high WBCS = infection), culture results are negative and no crystals Culture swab: cervical or urethral smears to rule out gonorrhea or confirm Chlamydia
32
Define/describe RA
chronic systemic inflammatory disease resulting in symmetrical joint pain and swelling as well as subsequent destruction of affected joints
33
Pathophysiology of RA
not well understood external trigger (infection, trauma) --> autoimmune reaction leading to synovial hypertrophy and chronic joint inflammation later stages include uncontrolled inflammation with pannus formation and subsequent cartilage and bone destruction (pannus = synovial membrane infiltrated w/ lymphocytes, plasma cells, macrophages; erodes and replaces underlying cartilage)
34
Presentation of RA
SYMMETRICAL initial symptoms develop over several weeks: stiffness, tenderness, pain with motion, swelling) prodrome of fever, fatigue, malaise and pain may precede loss of mobility acute episodes of polyarthritis may occur morning stiffness, often taking half an hour to regain motion in affected joints, difficulty performing ADLs
35
Risk factors for RA
female genetics (50% of risk) - first degree relative increases risk 2-3x positive HLA-DR4
36
PE findings for RA
deformities of hand and wrist: Boutonniere (non-reducible flexion PIP joint w/ hyperextension of DIP) Swan-neck deformity (hyperextension at PIP w/ flexion of DIP) Ulnar deviation of fingers and radial deviation of wrist rheumatoid nodules interosseous atrophy swollen, tender, warm joints when active dz NEVER affects DIP
37
Ddx for RA
``` OA fibromyalgia psoriatic arthritis SLE gout/septic arthritis ```
38
Imaging findings
x-rays used for detection and to monitor progression usually negative for first 6 months of condition marginal erosion will be earliest change look for: bilateral symmetry, periarticular soft tissue swelling, uniform joint space loss, juxta-articular osteoporosis, deformity, pseudocysts, C1-2 subluxation early: no destructive changes, may have osteoporosis moderate: periarticular osteoporosis, possible subchondral bone destruction, cartilage destruction, limited joint mobility, no joint deformities, muscle atrophy severe: cartilage and bone destruction evident, periarticular osteoporosis, joint deformity (subluxation, ulnar deviation, hyperextesnion) without fibrous or bony ankylosis, muscle atrophy extensive, soft-tissue lesions (nodules) terminal: fibrous or bony ankylosis, along with all from previous stage
39
Define/describe SLE
chronic, multifaceted autoimmune inflammatory disease that mainly involves the skin, joints, kidneys, blood cells and nervous system but can affect any organ system
40
Prognosis of SLE
isolated skin and msk involvement have higher survival rates than those w/ renal and CNS disease 50 fold higher risk for MI than healthy women SLE presentation can range from benign to emergency
41
Risks for SLE
female African descent genetic predisposition (HLA-B8, -DR2, -DR3)
42
Diagnosis of SLE
``` 4 of 11: SOAP BRAIN MD serositis (e.g. pericarditis) oral ulcers arthritis photosensitivity blood disorders (leukopenia, lymphopenia, thrombocytopenia, etc) renal involvement (proteinuria, etc) ANA immune: anti dsDNA, anti Smith, antiphospholipid (anticardiolipin) antibodies neuro (seizures, psychosis) malar rash discoid rash (raised rimmed lesions w/ keratotic scaling) ``` commonly will also have: fever, fatigue, weight change
43
Ddx for SLE
``` assess medications: chlorpormazine, methyldopa, hydralazine, procainamide, isoniazid, quinidine RA lyme fibromyalgia hepatitis C MS infectious mononucleosis lymphoma ```

Ortho (13 decks)

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