UWorld 1 Flashcards
(63 cards)
Fibromyalgia presentation
Most commonly in young to middle aged women with widespread pain, fatigue, and cognitive/mood disturbances.
Patients tend to have normal physical exam except for point tenderness in areas such as the mid trapezius, lateral epicondyle, costochondral junction in chest, and greater trochanter.
No specific lab findings. Diagnosed with widespread pain index and symptom severity scale rather than trigger points.
Fibromyalgia tx
Initial FM treatment should emphasize patient education, regular aerobic exercise, and good sleep hygiene.
Patients who do not respond to conservative measures may require meds. TCAs (amitriptyline) are 1st line. SNRIs (duloxetine, milnacipran) and pregabalin are alternate therapies that may be useful in patients not responding to TCAs.
Patients with persistent symptoms may need combo drug therapy, referral for supervised rehab, pain management or CBT.
Fibromyalgia dx
Widespread Pain Index (WPI). Score is 0-19. 1 for each spot.
1) Neck
2) Jaw (L and R)
3) Shoulder (L and R)
4) Upper arm (L and R)
5) Lower arm (L and R)
6) Chest
7) Abdomen
8) Upper back
9) Lower back
10) Hip (L and R)
11) Upper leg (L and R)
12) Lower leg (L and R)
Symptom Severity Scale (SSS). Score is 0-12.
1) Fatigue (0-3)
2) Waking unrefreshed (0-3)
3) Cognitive symptoms (0-3)
4) Somatice symptoms (0-3)
To dx FM you need:
1) WPI of at least 7 and SSS of at least 5. OR WPI of 3-6 and SSS of at least 9.
2) Symptoms present at similar level for 3 months
3) No disorder that would otherwise explain the pain
Manifestations of SLE
Clinical symptoms
1) Constitutional - fever, fatigue, and weight loss
2) Symmetric, migratory arthritis
3) Skin - butterfly rash and photosensitivity. painless oral ulcers.
4) Serositis - pleurisy, pericarditis, peritonitis
5) Thromboembolic events (due to vasculitis and antiphospholipid syndrome)
6) Neuro - cognitive dysfunction and seizures
Lab
1) Hemolyitc anemia, thrombocytopenia and leukopenia
2) Hypocomplementemia (C3 and C4)
3) Antibodies - ANA (sensitive). Anti-dsDNA and Anti-SM (specific)
4) Renal involvement - proteinuria and elevated Cr
Describe the typical joint manifestations of SLE
Arthritis and arthralgias affect 95%. They tend to be migratory, symmetric, polyarticular and are accompanied by brief morning stiffness (much shorter in duration than RA).
Knees, carpal joints, joints of fingers are most often affected. Joint pain often exceeds objective findings on exam. XRs usually show no evidence of joint destruction or erosion (unlike other inflammatory arthritides like RA)
Felty Syndrome
Advanced RA (usually longstanding over 10 years) associated with splenomegaly and neutropenia. Marked morning stiffness.
Diagnosis should not be made without neutropenia!
Behcet Disease
Presents with multiple oral and genital ulcers that are recurrent and painful. Uveitis is common.
Parvo infection - joint manifestation
In adults, most parvo infections are ASx or have flu-like symptoms. Minority of patients develop a symmetric, nonerosive arthritis or aplastic anemia.
These symptoms would not last longer than 3-4 weeks.
Disseminated gonococcal infection - describe the usual presentation
Polyarthralgia, skin lesions, and tenosynovitis. Morning stiffness is rare.
Clinical features of vertebral compression fracture
Causes
1) Trauma
2) Osteoporosis, osteomalacia
3) Infection (osteomyelitis)
4) Bone mets
5) Metabolic (hyperparathyroidism)
5) Paget Disease
Clinical pres
1) Chronic/gradual VCF - painless, progressive kyphosis, loss of stature
2) Acute VCF - low back pain and decreased spinal mobility, pain increasing with standing, walking, lying on back; tenderness at affected level. Can usually point to a specific event like lifting (or a bend, or a cough) where it started.
Complications
1) Increased risk for future fractures
2) Hyperkyphosis, possibily leading to protuberant adbdomen, early satiety, weight loss, decreased respiratory capacity
Absent ankle reflexes
Don’t need to be clinically signifiant. Patients over 70 often have this.
Spinal epidural abscess triad
Fever, severe localized back pain, and neuro defects (motor weakness, paresthesias, bowel/bladder dysfunction)
Lumbar spinal stenosis
Refers to a narrowing of the intraspinal canal, lateral recess, or neural foramen. Patients develop low back pain with neuro symptoms (sensory loss, weakness in legs) that is worse with spinal extension (walking, standing) but improved with leaning forward or lying down. Back pain persists when standing still.
Usually in patients over 60. Look out for pseudoclaudication. Vascular claudication is exertion-dependent and resolves when standing still.
Lumbosacral strain
Usually seen after a specific event or action. Patients typically have increased pain with movement and decreased pain with rest.
In addition, pain is in paraspinal area without significant tenderness to palpation of the vertebra
Lateral epicondylitis
Tennis elbow. Pain with supination or extension of the wrist and point tenderness just distal to the lateral epicondyle. From backhand in tennis or screwdriver use. Any activity with repeated forceful wrist extension and supination
Degeneration of extensor carpi radialis brevis tendon near lateral epicondyle.
Radial tunnel syndrome
Signs and symptoms similar to lateral epicondylitis and may occur in conjunction with it. Tenderness tends to overlie the extensor muscle wad
Pain is elicited by flexing the patient’s long finger while they are actively extending fingers and wrists.
Rupture of long head of biceps tendon
Causes pain in upper arm and shoulder and prominent bulge in midportion of upper arm.
Paget Disease of the bone (phases)
1) Osteolytic phase - osteoclast dominant.
2) Mixed phase - osteoclast plus osteoblast. Some new bone formation
3) Osteosclerotic phase - blasts dominant. Weak, thickened woven bone
Paget Disease of the bone overview
Patient with bone pain, HA, unilateral hearing loss and femoral bowing would be a typical presentation.
This is the most common bone disorder after osteoporosis (3% of adults over40). Characterized by focal increase in bone turnover, in which osteoclast dysfunction leads to bone breakdown and a compensatory increase in bone formation.
Pelvis, skull, spine and long bones are most commonly involved. Microscopic findings include increased numbers of abnormal appearing osteoclasts with a disorganized mosaic pattern of lamellar bone
Early stage lesions will have a lot of osteoclast activity, later progressing through a mixed phase, a predominantly osteoblastic phase and finally a residual sclerotic phase
Most patients are ASx and are identified incidentally by XR or elevated alk phos. Symptoms may include skeletal deformities, bone or joint pain, and fractures. Enlarging cranial bones may lead to increased hat size, HA, and hearing loss due to entrapment of CN8 or encroachment on the cochlea. Benign giant cell tumors of bone and osteosarcoma can also be seen
Avascular necrosis causes
1) Steroid use
2) Alcohol abuse
3) SLE
4) Antiphospholipid syndrome
5) Hemoglobinopathies (Sickle Cell)
6) Infections (osteomyelitis, HIV)
7) Renal transplant
8) Decompression sickness
Clinical manifestations, labs and imaging for Avascular necrosis
Clinical
1) Groin pain on weight bearing
2) Pain on hip abduction and internal rotation
3) No erythema, swelling or point tenderness
Labs
1) Normal WBC
2) Normal ESR and CRP
Rads
1) Crescent sign seen in advanced stage
2) MRI is most sensitive modality
Osteonecrosis
Caused by occlusion of end arteries supplying the femoral head, leading to necrosis and collapse of the periarticular bone and cartilage.
Osteonecrosis is common in patients with sickle cell disease due to disruption of microcirculation in the bone by sickling as well as increased intraosseous pressure due to bone marrow hyperplasia.
Femoral head has 2 main sources of blood - ascending arteries and the foveal artery, which lies within the ligamentum teres.
Foveal artery is open early in life, but may become obliterated in older patients. For this reason, aseptic necrosis of the femoral head is uncommon in children but the risk rises in older patients
Paget Disease - pathogenesis, labs, imaging and treatment
Pathogenesis - osteoclast dysfunction and increased bone turnover
Labs
1) Increased alk phos
2) Increased bone turnover markers (PINP, urine hydroxyproline)
3) Calcium and phosphorous are usually normal
Imaging
1) XR shows osteolytic or mixed lytic/sclerotic lesions
2) Bone scan shows focal increase in uptake
Tx - bisphosphonates
Polymyositis
Clinical presentation
1) Symmetrical proximal muscle weakness - often in lower extremities and slowly progressive (difficulty negotiating stairs or rising from seated position). Proximal arm weakness usually follows (trouble working with the arms overhead). Patients may develop dysphagia due to involvement of striated muscles of upper pharynx.
2) No/mild pain or muscle tenderness
3) Similar to dermatomyositis but without skin findings
Tests
1) Elevated muscle enzymes (CK, aldolase)
2) Autoantibodies (ANA, anti-Jo-1)
3) Bx (most definitive) - endomysial mononuclear infiltrate, patchy necrosis
Associated conditions
1) Interstitial lung disease
2) Myocarditis
3) Malignancy**
Tx
1) Systemic glucocorticoids
2) Glucocorticoid-sparing agents (methotrexate, azathioprine)