High Yield 5 Flashcards

1
Q

What is calcific tendonitis?

A

Calcium deposits within tendon
Pain related to impingement, inflammation, and increased intratendinous pressure from the calcific deposit

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2
Q

Sx + physical for calcific tendonitis

A

Hx
Localized pain
Gradual, atraumatic
Worse at night

Physical
Pain worse with AROM compared to PROM

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3
Q

Ix + management calcific tendonitis

A

XR + US show calcium deposits

Management
Often resolves spontaneously within 3-6mo
NSAIDs, steroid inj
Shockwave therapy
Therapeutic US
Heat

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4
Q

What is CRPS + what are the hallmark features?

A

Complex regional pain syndrome
Severe, continuing pain, disproportionate to any inciting event
Manifested by four clinical characteristics: based on Budapest criteria:
Intense pain
Vasomotor disturbances (temp or color changes)
Sudomotor (sweat glands) disturbances, as increased sweating or clammy skin
Motor or trophic changes (tremor, decreased ROM, weakness + hair, nail or skin changes)

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5
Q

RF for CRPS

A

Females
40-70S
Upper limb more common
Most report a triggering event (eg #, surgery, sprain)

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6
Q

Sx of CRPS

A

Progressive pain
Burning, throbbing
Sensitivity to cold, touch
Functional limitation

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7
Q

Physical for CRPS

A

Allodynia
Eedema
Color or temp changes
Thickening of skin
Joint contractures
Abnormal hair growth

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8
Q

Ix for CRPS

A

Sympathetic nerve blockage (lumbar block for lower extremity or stellate ganglion block for upper extremity)
Labs to exclude other systemic causes: CBC, ESR, fasting glucose, calcium, T4, TSH
Bone scan can show increased uptake
XRs can be initially normal then show patchy subchondral osteopenia + bone demineralization

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9
Q

Management of CRPS

A

Bisphosphonates
Short course steroids
Sympathetic nerve blockade
TCAs for pain relief
Gabapentin
Ketamine
Acupuncture
Physical therapy - Tactile desensitization, strengthening
Transcutaneous electrical nerve stimulation can be beneficial.
Behavioral management
Relaxation techniques
Stress management
Mirror therapy
Aerobic exercise
Somatosensory rehabilitation

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10
Q

What are the Spondyloarthropathies?

A

Ankylosing spondylitis (AS).
Reactive arthritis (ReA).
Psoriatic arthritis (PsA).
Arthritis associated with inflammatory bowel disease (IBD).
Juvenile onset spondyloarthritis.
Undifferentiated spondyloarthropathy (USpA)

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11
Q

RF for spondyloarthropathy

A

Male
Caucasian
Unprotected sex
Positive family history
ReA is significantly increased in persons with HIV.
More common in patients who were not breast fed
HLA-B27

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12
Q

RF for OA

A

Age
Fam hx
Obesity
Females
Joint injury
Impact sports
Abnormal biomechanics

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13
Q

Sx of OA

A

Insidious pain over years
Crepitus
Grinding
Stiffness <30mins after immobilization

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14
Q

Physical for OA (general, knees, hands, hips)

A

Joint line tenderness is common in hands and knees.
Joints may have crepitus, decreased range of motion (ROM), effusion, and atrophy of surrounding muscles.
In knees, involved compartments can include medial (most common), patellofemoral, and/or lateral, so accurate palpation is important. Effusion and trace joint warmth are common in acute flares.
In hands, may see nodules in the DIP and PIP joints, termed Heberden and Bouchard nodes, respectively
In hips, decreased and painful internal rotation are early signs, and tenderness over the anterior joint line is a later finding.

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15
Q

XR findings for OA generally, and XR views for thumb, hands, shoulder, knee + hip

A

X-ray characteristics include osteophytes, joint space narrowing, subchondral sclerosis, and cyst formation
Thumb CMC joint: true AP (Robert) view of the thumb, wrist AP, and oblique
Hands: AP and lateral
Shoulder: true glenohumeral AP (Grashey) view most sensitive
Knee: Weight-bearing AP in 20 to 45 degrees of flexion (Rosenberg view) is most sensitive and accurate for the medial and lateral compartments. Supine lateral and sunrise or merchant views are best for patellofemoral compartment.
Hip: Weight-bearing anteroposterior (AP) films are most sensitive.

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16
Q

Management of OA

A

Education
Set reasonable expectations on outcome (pain reduction, increased function, not cure).
Modification of activities to minimize pain and risk of joint trauma
Importance of nonpharmacologic therapies

Weight loss

Exercise
Aquatic and low-impact land-based aerobic exercise, strength training, and ROM exercise

Mood + sleep management

Meds
Topical NSAIDs
Oral NSAIDs
Duloxetine

Injections
PRP
Viscosupplementation with hyaluronate
Steroid inj - usually lasts 2-4 wks. Max 4 inj per year
Possible stem cell inj

Surgery
When “bone on bone”
Debridement or osteotomy
Joint replacement

Other
Bracing
Heat/ ice
TENS
RMT
Acupuncture
Walking aids

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17
Q

What should be discouraged in management of OA?

A

Glucosamine supplements
Visco supplements
Opioids
Repeat steroid injections
Arthroscopy

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18
Q

What is osteochondritis dissecans?

A

Osteonecrosis of a fragment of subchondral bone + cartilage, which can break off and cause pain, swelling + joint dysfunction

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19
Q

What are the common places osteochondritis dissecans affects?

A

Knee (lateral aspect of medial femoral condyle)
Ankle (talar dome)
Elbow (humeral capitellum)

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20
Q

RF for osteochondritis dissecans

A

Typically 12-19y/o
Boys more common
OCD in one joint is a RF for contralateral joint
Sports involving jumping, pivoting, cutting movements
Sports with repetitive loading of the elbows, such as baseball and gymnastics, are specific risk factors for OCD of the elbow.

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21
Q

Sx of osteochondritis dissecans

A

Vague, insidious, poorly localized pain
Can have swelling + stiffness
Can have locking/ catching sensation
Hx of ankle sprain, not responding to therapy 4-6 wks after injury

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22
Q

Physical for osteochondritis dissecans

A

Decreased or painful ROM
Joint line tenderness
Wilson’s sign - flex the knee to 90 deg, internally rotate the tibia and extend the knee slowly, watching for a painful response and pain is then relieved by external rotation

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23
Q

Ix for osteochondritis dissecans

A

XR
Characteristic appearance on x-ray is a well-circumscribed lucent defect in subchondral bone that may or may not contain an internal bone density

MRI
Arthroscopy is gold standard

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24
Q

DDx for osteochondritis dissecans

A

Fracture
Ligamentous or cartilage injury
Tendinosis
Inflammatory arthropathy
Mechanical issue (i.e., patellofemoral pain syndrome)
Juvenile: apophyseal injury
Adult: osteoarthritis

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25
Management + RTP of osteochondritis dissecans
If asymptomatic, incidental finding = monitor until radiographic healing If symptomatic, stable (not displaced): relative rest, non wt bearing if lower limb, consider bracing or casting, physio for strengthening If symptomatic, unstable (displaced lesion) or failed conservative management: refer to ortho for fixation/ debridement/ microfracture Refer all adults to ortho RTP 3-4mo
26
DDx for hypermobility
Ehlers-Danlos syndrome classic type Marfan syndrome Osteogenesis imperfecta Loeys-Dietz syndrome Ankylosing spondylitis Rheumatoid arthritis Fibromyalgia Multiple sclerosis Amyotrophic lateral sclerosis Autonomic polyneuropathies Myopathy Chronic fatigue syndrome
27
Management of hypermobility
PT OT Splints, orthotics
28
RF for hypermobility
Females Children + teens
29
Medical conditions that correlate w/ hypermobility
Recurrent joint subluxation and dislocation Pes planus Chronic pain Anxiety and depression Gastroesophageal reflux disease (GERD) Irritable bowel syndrome (IBS) Syncope Orthostatic hypotension
30
What is osteoporosis?
Systemic disorder characterized by decreased bone mass and microarchitectural deterioration of bone leading to bone fragility and increased susceptibility to fractures of the hip, spine, and wrist
31
What is osteopenia vs osteoporosis?
Osteopenia (low bone mass): Bone mineral density (BMD) defined as T-score between −1.0 and −2.5 standard deviation (SD) below the mean of a young adult reference population on dual energy x-ray absorptiometry (DEXA) scan Osteoporosis (decreased bone mass): BMD T-score ≤2.5 SD below the mean of a young adult reference population
32
Types of osteoporosis
Primary: age-related (postmenopausal estrogen deficiency, age-related vitamin D deficiency) Secondary: (drug or concurrent medical condition etiology)
33
Hx + Ix for osteoporosis
Hx Low trauma # Height loss Investigations DEXA T + L spine to evaluate for #
34
Management of osteoporosis
Bisphosphonates Inhibit osteoblast + osteoclast activity SE: N/V, abdo pain, esophagitis, osteonecrosis of jaw OR denosumab Exercise + balance therapy Repeat BMD q2yrs
35
Prevention of osteoporosis
Identify + treat secondary causes Vit D + calcium supplement
36
RF for osteoporosis
Female sex Parental history of osteoporotic hip fracture Personal history of fracture Age 65 yr or older Low body weight Diet low in calcium; low in vitamins C, D, and K; and decreased copper, manganese, and zinc mineral content Estrogen deficiency: postmenopausal or premenopausal secondary to over exercising and/or eating disorder Sedentary lifestyle, lack of weight-bearing exercise History of falls Female athlete triad: low energy availability (EA) (with or without disordered eating), menstrual dysfunction, low BMD Medications: glucocorticoids, anticonvulsants, cancer chemo drugs, thyroid replacement drugs, proton pump inhibitors (PPIs) Excessive alcohol Smoking Other diseases: diabetes, hyperparathyroidism, hyperthyroidism, multiple myeloma, rheumatoid arthritis Impaired absorption of calcium, phosphate, and vitamin D from the gastrointestinal (GI) tract, as in inflammatory bowel disease, gastrectomy, celiac disease, jejunoileal bypass, or pancreatic insufficiency
37
What is myofascial pain syndrome?
Myofascial trigger points are “knots” in muscle that cause pain MPS is >1 MTP
38
Sx + physical for myofascial pain syndrome
Hx Vague, persistent or intermittent pain Can be uni or bilateral Physical criteria for diagnosis Palpation of taut band Tender in taut band Reproduction of index pain w/ sustained pressure on MTP
39
RF for myofascial pain syndrome
Poor posture Overuse Repetitive motion Deconditioned muscle Prolonged sitting
40
Management of myofascial pain syndrome
Address biomechanical factors Dry needling, trigger point inj, acupuncture
41
Sx + physical exam for fibromyalgia
Sx Widespread, symmetrical pain Poor sleep, fatigue Associated w/ myofascial pain Exam Tenderness in multiple soft tissue locations
42
What is a stress #?
Damage d/t repetitive loading that exceeds healing capacity Can range from mild periosteal reaction to displaced #
43
What are low vs high risk stress #?
Low risk = pelvic, femoral shaft, posteromedial tibia, fibula, metatarsal shafts, cuboid, calcaneus, and cuneiform High risk = femoral neck (FNSF), anterior tibial shaft (ATSF), patella, medial malleolus, 2nd metatarsal base, proximal 5th metatarsal, sesamoids, tarsal navicular, and talus
44
RF for stress #
Female gender Female body mass index (BMI) <19 Late menarche ≥15 yr Prior SF Extreme pes cavus or planus >5 degrees knee valgus/external rotation (ER) Inadequate caloric intake Excessive caffeine, alcohol, or tobacco use Amenorrhea/oligomenorrhea Osteopenia Chronic corticosteroid use Rapid increase in training volume Recreational runners >25 miles per week Poor footwear Running on hard surfaces Low 25-hydroxyvitamin D Low testosterone (males)
45
Sx of stress #
Insidious pain w/ repetitive activity Pain at rest Ask about RF, nutrition, steroid use, menses
46
Physical for stress #
Direct bony tenderness +/- edema Tender “N” spot (dorsal central third of the navicular bone between the anterior tibial and hallucis longus tendons) suggestive of SF Calcaneal squeeze test: simultaneous pressure on the medial and lateral aspects of calcaneus, pain suggestive of SF Fulcrum test: pain at the site with bending the long bone over a table edge or examiner’s leg or forearm; useful for tibial and FSSF Log roll test: Passive internal rotation (IR)/ER of the thigh elicits groin pain in an FNSF. Patellar-pubic percussion test: Place stethoscope on the ipsilateral pubic tubercle and percuss the ipsilateral patella or use a tuning fork; the sound is reduced on the side in which an FNSF is present. Flamingo test: Patient stands on the affected side. A positive test is indicated by pain in the location of the SF; useful for FNSF, FSSF, lower leg, and sacral SF Tuning fork test: pain when applying a 128-Hz tuning fork over the site of suspected SF; useful for tibia and fibula SFs
47
Ix for stress #
XR, repeat in 2-3 wks if normal Lucency or callus formation visible Bone scan MRI is gold standard Labs: vitamin D, CBC, chem 7, calcium, TSH, albumin, prealbumin, phosphate, and parathyroid hormone Females with menstrual dysfunction: FSH, LH, estradiol, testosterone, HCG Dexamethasone suppression test if excess cortisol suspected
48
DDx for stress #
Muscle strain/tendinopathy Fasciitis/periostitis Exertional compartment syndrome Nerve/artery entrapment Bone tumor FNSF may mimic adductor or hip flexor strain. ATSF can be confused with shin splints. Medial tibial SF can mimic anserine bursitis.
49
Management of stress # (general)
Relative rest Cast/ boot/ crutches to ensure pain free rest Compression boot for tibial SF NSAIDs Refer to ortho for high risk SF Shock wave therapy FU q2-4 wks Nutrition: ​​Adequate calories, protein, and carbohydrates for age; body type and sport Daily calcium 2,000 mg and vitamin D 800 IU 50,000 IU vitamin D weekly ×12 if deficient
50
Complications of stress #
Complete fracture, delayed union, nonunion, avascular necrosis
51
Prevention of stress #
Adequate calories and nutrition 1,500 to 2,000 mg calcium and 800 IU vitamin D per day Screen for female athlete triad. Padded insoles and orthotics (military recruits) Replace footwear after 6 mo or 300 miles. Limit training increase to 10% per week (intensity, duration, frequency).
52
Sport that causes stress fracture of coracoid process
Trapshooting
53
Sport that causes stress fracture of Scapula
Running with hand weights
54
Sport that causes stress fracture of humerus
Throwing, racket sports
55
Sport that causes stress fracture of olecranon
Throwing, pitching
56
Sport that causes stress fracture of ulna
Racket sports, gymnastics, volleyball, swimming, wheelchair sports
57
Sport that causes stress fracture of Pars interarticularis
Gymnastics, ballet, cricket fast bowling, volleyball, spring board diving
58
Sport that causes stress fracture of Pubic ramus, femur
Distance running, ballet
59
Sport that causes stress fracture of Tibia
Running
60
Sport that causes stress fracture of fibula
Running, ballet, aerobics
61
Sport that causes stress fracture of Medial malleolus
Running, basketball
62
Sport that causes stress fracture of talus
Pole vaulting
63
Sport that causes stress fracture of navicular
Sprinting, mid distance running, handling, long jump, triple jump, football
64
Sport that causes stress fracture of base of second metatarsal
Ballet
65
Sport that causes stress fracture of 5th metatarsal
Tennis, ballet
66
Sport that causes stress fracture of Sesamoid bone
Running, ballet, basketball, skating
67
Management of femoral neck stress fracture
Bed rest for one week then gradual weight-bearing if non-displaced, if displaced needs surgical fixation
68
Management of anterior tibia fracture
Non-weightbearing on crutches for six weeks or screw fixation
69
Management of medial malleolus stress fracture
Non-wt bearing cast immobilisation for six weeks or surgical fixation
70
Management of talus stress fracture
Non-wt bearing cast immobilisation for six weeks or surgical fixation
71
Management of navicular stress fracture
Non-weight bearing cast immobilisation for six weeks or surgical fixation
72
Management of base of 5th metatarsal stress fracture
Cast immobilisation
73
Management of base of 2nd metatarsal stress fracture
Non-wt bearing x2 wks then partial wt bearing x2 wks
74
Management of sesamoid stress fracture
Non wt bearing x4 wks
75
What is myositis ossificans?
A localized heterotopic ossification that develops in muscle from physical trauma Anterior muscle groups of the thigh and arm are most frequently affected but may occur at any site Osteoblasts proliferate inappropriately in a healing muscle hematoma and lay down bone over a period of weeks to months. Bone maturation usually takes 6 to 12 mo to complete. Once ossification takes place, little can be done to accelerate the resorptive process, which may take months to years. Average duration of symptoms related to myositis ossificans (MO) is 1.1 yr.
76
RF for myositis ossificans
Contact sports Application of heat or massage to injury site Premature return to activity Reduced range of motion of injured muscle Previous muscle injury Delay in treatment >3 days Adjacent joint effusion
77
Sx of myositis ossificans
Pain, stiffness, weakness, decreased muscle mass Night pain Signs of MO present 2-3wks post injury - presents as unresponsive to treatment
78
Physical for myositis ossificans
Initially, may palpate a doughy mass at 1 to 2 wk that gradually becomes indurated Persistent tenderness to palpation with local edema that fails to resolve Reduced range of motion that worsens 2 to 3 wk after injury
79
Ix for myositis ossificans
US detects calcifications within 2 wks of injury XR detects calcifications within 3-4 wks of injury Bone scan will show if it is fully developed
80
DDx for myositis ossificans
Muscle contusion Muscle or tendon tear Fracture Malignant neoplasm: osteosarcoma, lymphoma, or rhabdomyosarcoma Compartment syndrome Abscess Rhabdomyolysis
81
Management of myositis ossificans
Self limiting RICE Non painful passive stretching + strengthening Shock wave therapy RTP usually 3-6mo Sx can persist for >1yr
82
Prevention of myositis ossificans when contusion occurs
Immobilize muscle in slight tension (i.e. slightly flexed knee for quad injury) for 24 hrs Rest, ice, compression, elevation Avoid soft tissue therapy in firt 24hrs NSAIDs
83
What primary cancers metastasize to bone?
Lung, breast, prostate ϲaոϲеr, and multiple myеlοma
84
What imaging to use for ?lytic lesion?
Bone scan In multiple myeloma, whole body MRI often used
85
Types of Benign bone tumors
Osteoid Osteoma Osteoblastoma Enchondroma Chondroblastoma Giant Cell Tumor of Bone Osteochondroma Fibrous Dysplasia Aneurysmal Bone Cyst
86
Types of malignant bone tumors
Osteosarcoma Chondrosarcoma Ewing Sarcoma Malignant Fibrous Histiocytoma of Bone Fibrosarcoma of Bone Multiple Myeloma Lymphoma of Bone Metastatic Bone Disease
87
Types of benign soft tissue tumors
Lipomas Hemangiomas Schwannomas and Neurofibromas Fibromas Leiomyomas Myxomas
88
types of malignant soft tissue tumor
Desmoid Tumors (Aggressive Fibromatosis) Giant Cell Tumor of Tendon Sheath Pigmented Villonodular Synovitis (PVNS) Liposarcoma Rhabdomyosarcoma Leiomyosarcoma Synovial Sarcoma Angiosarcoma Malignant Peripheral Nerve Sheath Tumor (MPNST) Fibrosarcoma Epithelioid Sarcoma Undifferentiated Pleomorphic Sarcoma (UPS)
89
What is gout?
Inflammatory deposition of monosodium urate crystals
90
Stages of gout
Acute phase: inflammatory monarthritis; resolves within several days to just over a week Interval phase: The patient is asymptomatic. Chronic phase: intermittent repeated flairs of monarticular or polyarticular gout and soft tissue deposition of tophi
91
Common joints affected by gout
1st metatarsophalangeal (MTP) joint (most common site of initial presentation; also known as podagra), olecranon, ankle, wrist, knee, tarsal joints, and interphalangeal joints of the hand
92
RF for gout
Male Dehydration Pacific islander Excessive alcohol intake (especially beer and liquor) Hypertension and cardiovascular disease Chronic diuretic use (thiazide and loop) Organ transplant recipients treated with calcineurin inhibitors Recent surgery Hyperuricemic state (from either overproduction or underexcretion of uric acid) Rapid changes in uric acid level Diets high in purine-containing products Diets low in dairy or high in meat or fish
93
Sx + physical for gout + signs of tophi
Severely painful, erythematous, and swollen joint (noninfectious monarthritis) Pain at its max at 24-48 hrs Physical Gout: Swelling, erythema, warmth, and tenderness of affected joint 80% of flares involve a single joint (1st MTP, knee, ankle, and other joints). Sometimes overlying skin can be erythematous and desquamated, resembling cellulitis. Tophi: Subcutaneous nodules (resembling rheumatoid arthritis) or a bulky mass overlying a joint ± Tenderness or erythema of tophi Aspirated tophi contents appear as white pasty or chalky material.
94
Ix for gout
Labs: CBC, CRP, uric acid (can be normal) Joint aspirate Gout: needle-shaped, negatively birefringent monosodium urate crystals are seen under polarized light microscopy. CPPD (pseudogout): rhomboid-shaped crystals with weakly positive birefringence
95
DDx for gout
Pseudogout Rheumatoid arthritis Septic arthritis Osteoarthritis Reactive arthritis Osteomyelitis Malignancy Joint trauma
96
Management of gout
NSAIDs (naproxen 500mg BID or indomethacin 50mg TID) x3-10 days Oral prednisone 40mg x2-3 days then taper Intra-articular steroid injections Colchicine 0.6mg BID
97
Prevention of gout
Minimize alcohol Minimize meat + seafood Increase dairy Minimize diuretic use Urate lowering meds
98
Indications for preventative meds in gout, + when to start
Recurrent or disabling gout attacks (specifically >2 gout attacks per year). Persistent tophi. Joint damage noted on imaging. Uric acid nephropathy or nephrolithiasis Wait 2-6 wks after acute attack Allopurinol 100mg, titrate up to target uric acid <6 Febuxostat is alternative for those w/ renal failure
99
What is pseudogout?
Calcium pyrophosphate deposition disease (CPPD)
100
RF for pseudogout
Gout (20% may be hyperuricemic) Hemochromatosis Hypothyroidism Trauma Osteoarthritis Hyperparathyroidism Hemosiderosis Hypophosphatasia Hypomagnesemia Aging Amyloidosis
101
Sx of pseudogout
Acute joint swelling in one or more joints with previous episodes involving the same joint (characteristic of crystal arthropathies) The most common joint is the knee, followed by the wrist, shoulder, and hip. May be severe and associated with malaise and fever Period of previous episodes (typically several days to weeks) Patients often are symptom-free between attacks.
102
Physical for pseudogout
Warmth Edema/effusion Tender Limited range of motion
103
Ix for pseudogout
Synovial fluid microscopy ​​weakly positive birefringent rhomboidal-shaped crystals XRs show calcium deposition Once dx, check calcium, magnesium, thyroid-stimulating hormone, ferritin, transferrin, iron, phosphorus, and alkaline phosphatase levels
104
DDx for pseudogout
Gout (can coexist) Septic arthritis (can coexist) Rheumatoid arthritis Osteoarthritis Trauma (hemarthrosis) Human leukocyte antigen B27–related peripheral arthritis (psoriatic arthritis, ankylosing spondylitis, reactive arthritis)
105
Management of pseudogout
Joint aspiration Intra-articular steroid inj Joint rest, splinting NSAIDs Colchicine 2nd line
106
Prevention of pseudogout
Colchicine 0.6mg BID for recurrent attacks
107
Sx + hx qs for rheumatoid arthritis
​​Polyarthritis most commonly affecting the joints of the wrist, the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of the hands, and the metatarsophalangeal (MTP) joints of the feet Warmth, swelling, tenderness Stiffness in AM >1 hr, improves w/ activity Progression to joint destruction and deformities (ulnar deviation at MCPs, volar subluxation at MCPs and wrists, swan-neck, and/or boutonnière deformities of fingers) Constitutional symptoms are very common (e.g., low-grade fever, fatigue, myalgia, weight loss) Extra-articular manifestations: anemia, rheumatoid nodules (20–30%), pleuritis, pericarditis, entrapment neuropathies (carpal tunnel syndrome), episcleritis and scleritis (<1%), splenomegaly, renal disease, interstitial lung fibrosis, pericarditis, interstitial lung disease, vasculitis, Sjögren syndrome, Felty syndrome (rheumatoid arthritis [RA], splenomegaly, neutropenia)
108
RF for rheumatoid arthritis
Female gender (Pregnancy and oral contraceptive use may be protective.) Nulliparity Family history (identical twins 3 to 4 times more likely to share disease than fraternal twins) Human leukocyte antigen (HLA)-DR4 (also tend to have more severe disease) Cigarette smoking Silica or asbestos exposure Electrical workers Wood workers
109
Physical for rheumatoid arthritis
​​Examine joints thoroughly for synovitis (warmth, swelling, tenderness, erythema). Look for deformities (swan-neck, boutonnières, ulnar deviation of digits/wrists, volar subluxation at MCP or wrist) Nail fold infarcts Splinter hemorrhages Rheumatoid nodules Splenomegaly Pericardial rub Pleural effusions
110
Ix for rheumatoid arthritis
Joint fluid exam 10,000 white blood cells (WBCs) with neutrophilic predominance characteristic but nondiagnostic RF positive in 80% Anti-CCP Low Hb, high leuks, high platelets, low albumin, high ALP XR Erosions or bony decalcification CT or MRI
111
DDx for rheumatoid arthritis
Systemic lupus erythematosus (SLE) Osteoarthritis (typically involves distal interphalangeals, knees, hips) Reactive arthritis Lyme disease Gout Pseudogout Polymyalgia rheumatica Hypothyroidism Hypertrophic osteoarthropathy Colitis Ankylosing spondylitis
112
Management of rheumatoid arthritis
Education, relative rest, exercise, PT, OT, CBT Strength training + aerobic exercise Fish oil Limit CV RF DMARDs Methotrexate - works within 4 wks not to take in pregnancy monitor for hematologic, hepatic, or pulmonary side effects use folic acid supplementation 1 mg daily with methotrexate If fails, combine therapy with other DMARDs (methotrexate + sulfasalazine + hydroxychloroquine) or a biologic agent with or without methotrexate Sulfasalazine Hydroxychloroquine Minocycline Azathioprine TNFi - etanercept, infliximab Steroids
113
Complications of rheumatoid arthritis
Increased risk of CV disease + stroke Increased risk of infection Increased risk of lymphoma
114
What features suggest an inflammatory disorder?
Insidious onset Prolonged stiffness after rest Pain worse at night. Improvement with motor activity Fever, weight loss. Raised to CRP Good response to NSAIDs
115
Differential diagnosis for atraumatic single swollen joint
Septic arthritis, gout, pseudo gout, Lyme disease, reactive or psoriatic arthritis, osteoarthritis, malignancy (synovial sarcoma), rheumatoid arthritis, sarcoidosis, haemophilia
116
Differential diagnosis for atraumatic polyarthritis (pain + swelling)
Rheumatoid arthritis, viral arthritis (EBV, parvo virus), psoriatic or reactive arthritis, inflammatory osteoarthritis, SLE, rheumatic fever, haemachromatosis, Sjögren’s syndrome
117
Differential diagnosis for polyarthralgia (joint pain without swelling)
Drug induced (quinolones, acyclovir, vitamin A, beta blockers, statins) Viral infection, thyroid disease, parathyroid disease, PMR, inflammatory myositis, leukaemia, depression, somatisation, fibromyalgia
118
What is the work up for Lyme disease?
Enzyme immunoassay and Western blot.
119
Hx qs for syncope
Before: events leading up to syncope, prodrome Lightheadedness, nausea, tunnel vision During exertion (?cardiac) or after (?non cardiac) During LOC time After Mental state - groggy (?non cardiac) vs alert (?cardiac) r/o seizure (tongue biting, jerking, incontinence) Fam hx
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Physical on sideline for syncope
Check BP both arms Consider rectal temp Full neuro eval Glucose
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Physical in office for syncope
Orthostatic vitals Cardiac exam - standing, supine + supine w/ valsalva Neuro exam
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Ix for syncope
ECG Labs - CBC, TSH, glucose Echo Holter Stress testing
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DDx for syncope
Cardiac causes (usually occurs during exertion): Anomalous coronary artery Arrythmogenic right ventricular cardiomyopathy (ARVC) Brugada syndrome Catecholaminergic polymorphic ventricular tachycardia (CPVT) Coronary artery disease HCM LQTS Myocarditis Right ventricular outflow tract ventricular tachycardia Severe aortic valve stenosis Non cardiac causes (usually after or not related to exertion) Drug abuse Heat stroke Hypoglycemia Hyponatremia Orthostatic hypotension Seizure Vasovagal syncope
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Prevention of syncope
Education regarding warm up + cool down Proper nutrition + hydration Appropriate clothing
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What is rhabdomyolysis?
Breakdown + necrosis of skeletal muscle w/ release of CK + myoglobin Combination of myoglobinuria, hypovolemia, and aciduria may lead to acute renal disease Can be result of trauma/crush injury or as a result of training error where exertion persists beyond the point of fatigue (exertional rhabdomyolysis [ER]), often due to novel activity
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RF for rhabdomyolysis
Sudden increase in exercise intensity and repetitive muscular loading Inadequate conditioning Poor hydration Exercise in high heat or humidity Stimulant and supplement use (phentermine, creatine) High body mass High-risk medication or drug use (cocaine, amphetamines, alcohol, nonsteroidal anti-inflammatory drugs [NSAIDs], antihistamines, statins, etc.) Ongoing infection/exercise while febrile Sickle cell trait Heritable muscle enzyme deficiencies
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Sx of rhabdomyolysis
Muscle pain, weakness, dark urine Fever, tachycardia, nausea Malaise
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Physical for rhabdomyolysis
Muscle tenderness, swelling, weakness Hypovolemic state Decreased urine output
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Ix for rhabdomyolysis (initially + once resolved)
CK 5-10 times upper limit of normal UA - positive for heme but absent RBCs suggested myoglobinuria Other labs: CBC, K+, Na+, Ph, uric acid, Ca Once rhabdo is resolved, to determine if genetically causes, do forearm ischemic test Obtain baseline ammonia and lactic acid levels. Inflate sphygmomanometer to >200 mm Hg. Patient performs hand-grip exercises to fatigue. Cuff is removed and serial blood tests are drawn. Minimal or no rise in lactic acid suggests carbohydrate metabolism disorder or McArdle disease. Delayed rise or no rise in the ammonia level suggests myoadenylate deaminase deficiency. Normal rise in ammonia and lactic acid levels suggests the presence of a disorder of lipid metabolism. Muscle biopsy + genetic testing if ?underlying genetic condition
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DDx for rhabdomyolysis
Muscle strain Delayed onset muscle soreness Muscle infection Sickle cell crisis Nontraumatic myopathies Hypercalcemia/hyperparathyroidism Hypo/hyperthyroidism
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Management of rhabdomyolysis
Aggressive fluid resus w/ isotonic saline Bicarb administration Treat underlying cause
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Complications (early + late) of rhabdomyolysis
Early complications: Hyperkalemia Hypocalcemia Cardiac arrhythmia Cardiac arrest Compartment syndrome Late complications (past 12 hr): ARF with oliguria Hypercalcemia Disseminated intravascular coagulation Compartment syndrome
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Sx of hypoglycemia + glucose reading
Sweating, HA, tremor, hunger, altered LOC <3.6
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Management of hypoglycemia
glucose gel in buccal mucosa or glucagon 1mg IM If sx resolve w/ glucagon, give long acting carb and monitor glucose frequently
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Prevention of hypoglycemia w/ exercise
Inform diabetic athletes about signs of hypoglycemia Have 15g of sugar when exercising (1.5 cup fruit juice) Check blood sugar before + after exercise Warm up for 15 mins before intense exercise Consider reducing insulin dose prior to exercise
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What is REDS?
Dietary intake is insufficient for energy expenditure (problematic low energy availability)
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Hx qs to ask for REDS
Diet Food restriction Menstruation Irregular menses Delayed onset of menses Exercise Excessive exercise beyond recommended amount Reduced performance Injuries Hx of stress # Exercising while injured Recurrent injuries Prolonged recovery Mental health Body image Fear of weight gain Life stressors Low mood Other sx Persistent fatigue Cold intolerance Constipation Hair loss, dry skin
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Physical for REDS
Ht, wt, BMI Orthostatic vitals Hair, skin, nails Thyroid exam Cardiac exam Consider pelvic exam if amenorrhea
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Ix for REDS
Labs - CBC, lytes, iron, TSH, prolactin (normal) T3 - low LH + FSH (low or normal) estrogen (low) cortisol (mildly elevated) Low IGF-1  Low glucose  Low insulin  Low testosterone  Low T3  High LDL or total cholesterol   PT DEXA if stress #
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DDx for REDS
Pregnancy Pituitary disease Hyperthyroidism Hypogonadism Hyperparathyroidism Primary ovarian insufficiency Polycystic ovarian syndrome Adrenal dysfunction Autoimmune disease Anabolic steroid use/abuse Excess glucocorticoid administration Malabsorption syndromes
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RF for REDS
Low self esteem Tendency towards perfectionism Sports that promote leanness (gymnastics, figure skating, ballet, diving, swimming, XC running) Veggie Early sport specific training Prolonged exercise periods Dieting
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Management of REDS
Education Increase energy intake Reduce exercise Energy rich supplement Address underlying mental health dx (CBT, antidepressants for comorbid anxiety/ depression) Calcium 1500mg/ day Vit D 1000 IU/ day Activity modification recommendations + home exercises Rest days High impact loading + resistance training to support BMD Referrals RD Sports psychologist S+C Use CAT2 calculator to determine risk + management
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Complications of REDS
Infertility Decreased BMD Iron deficiency Increased risk of illness + injury Stress # Depression + anxiety Decreased strength + endurance Decreased concentration + coordinati
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Prevention of REDS
Education on RED-S, healthy eating Reduce emphasis on weight Promote that good performance doesn’t necessarily mean a healthy athlete Screen for RED-S in PPE
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What qs to ask in infertility/ abnormal menses?
Menstrual hx Cycle length LMP Age of menarche Frequency + duration of menses Past irregularity Prev pregnancies Sexual activity Contraception PMH Training Overtraining Diet Eating disorders Calcium intake Injuries Stress # Androgen excess, abnormal thyroid, pituitary disorders: Hair growth, acne Temp intolerance, palps, bowel changes, tremor, mood changes, skin HA, galactorrhea Changes in weight Psychosocial stressors Meds + drugs
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Physical for infertility/ abnormal menses
BP, HR Ht, wt, body fat % Skin + hair Thyroid exam Pelvic exam
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Ix for infertility/ abnormal menses
bHCG TSH, T4 FSH, LH Prolactin, total + free testosterone, estrogen Pelvic US Head MRI for ?pituitary tumor Male factors
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DDx for infertility/ abnormal menses
Hypothalamic dysfunction: Functional hypothalamic amenorrhea: Energy deficiency–related amenorrhea secondary to excessive exercise, weight loss, disordered eating Primary gonadotropin-releasing hormone (GnRH) deficiency: Congenital disorders such as Kallmann syndrome Secondary/acquired GnRH deficiency: Traumatic brain injury, brain tumor Physiologic: Pregnancy Hormonal contraception Menopause Pituitary dysfunction: Hyperprolactinemia Prolactinoma Cushing syndrome Empty sella syndrome Sheehan syndrome Autoimmune disease Medications Anatomic abnormality/outflow tract obstruction: Congenital: müllerian agenesis, imperforate hymen, transverse vaginal septum, androgen insensitivity Acquired: Asherman syndrome Primary ovarian insufficiency: Congenital: gonadal dysgenesis, Turner syndrome Acquired: ovarian neoplasm, ovarian destruction secondary to medications, radiation, autoimmune disorder Other endocrine gland dysfunction: Thyroid dysfunction Polycystic ovary syndrome (PCOS) Adrenal dysfunction
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Management of infertility
Chart cycle, intercourse, training Functional hypothalamic amenorrhea Reduce training Increase body wt Calcium + vit D
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What is oligomenorrhea?
Menstrual cycles >35 days, no perceptible s
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What is amenorrhea?
No menstrual cycle >3mo
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What is primary amenorrhea?
>15 y/o no periodW
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What is PARmed-X?
screening tool to identify high risk pts, there is a regular one and a pregnancy specific one (prior spontaneous abortion, placenta previa, spotting, incompetent cervix, triplets, medical conditions) provides prescription exercise program in pregnancy
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What advice can you give for exercise during pregnancy?
Avoid exercise lying on back from 16 wks onwards Avoid exercise in warm or humid conditions Avoid breath holding exercise Avoid contact sport or sport w/ high risk of falling
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What are Warning signs to stop exercise in pregnancy?
Vaginal bleeding Dyspnea prior to exertion Dizziness Headache Chest pain Muscle weakness Calf pain or swelling Preterm labor Decreased fetal movements Amniotic fluid leakage
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What are Absolute CI to exercise in pregnancy?
Incompetent cervix Intrauterine growth restriction (IUGR) Multiple gestations (more than triplets) Persistent 2nd- or 3rd-trimester bleeding Placenta previa after 25 to 28 wk of gestation Preeclampsia Pregnancy-induced hypertension (HTN) Premature labor during current or prior pregnancy Premature rupture of membranes Risk of premature labor
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What are common MSK issues in pregnancy?
Carpal tunnel syndrome De Quervain tenosynovitis Lower back + pelvic pain Femoral head osteonecrosis Usually occurs late in pregnancy or after delivery Sx: antalgic gait, pain at rest, painful ROM Rx: restricted wt bearing, avoid surgery til after delivery Transient osteoporosis Sx: antalgic gait, pain w/ activity but not at rest, usually 3rd trimester Rx: protected wt bearing
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What are the best forms of exercise during pregnancy?
Swimming Stationary cycling Weight training Walking
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Positive effects of exercise during pregnancy
potential risk reduction for development of GDM, pregnancy-induced HTN, and preeclampsia a decrease in postpartum depression symptoms decreased incidence of urinary incontinence
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Sx of altitude sickness + onset
usually onset within 12-24hrs and self limited Nausea Light-headedness Headache Insomnia Anorexia Malaise Fatigue Weakness Impaired memory Inability to focus or concentrate
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Sx + onset of HAPE
Symptoms of AMS may present initially and then progress 2 to 5 days after ascent to dyspnea on exertion and/or dyspnea at rest: Persistent cough, progressing to pink, foamy sputum Chest tightness Fatigue Muscle weakness
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Sx of HACE
HACE: Ataxia Confusion Headache Vomiting Disorientation Irrational behavior Auditory or visual hallucination Lethargy Altered level of consciousness Unconsciousness or coma within 24 hr after the onset of ataxia
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RF for altitude sickness
Low pressure front, winter Rapid ascent Sleeping at altitude >2,000 m; exceeding >500 m/day sleeping altitude above 2,500 m Lack of acclimatization Young age Strenuous exertion at high altitude Previous history and/or individual susceptibility to altitude illness Obesity Chronic obstructive pulmonary disease, sickle cell disease, uncompensated congestive heart failure, or pulmonary hypertension
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Signs of AMS on exam
usually normal, potentially tachy or bradycardic
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Signs of HAPE on exam
Breathlessness at rest Cyanosis Crackles in right middle lobe are typical but can be anywhere in the lung field. Tachycardia Tachypnea Low-grade fever Orthopnea
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Signs of HACE on exam
Inability to perform activities such as dressing or eating Truncal ataxia demonstrated by poor heel-toe walking Mental status changes Occasionally focal neurologic deficits Funduscopic examination can demonstrate papilledema and retinal hemorrhages
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DDx of AMS
Dehydration Exhaustion Viral syndrome Gastroenteritis Hangover Hypothermia Carbon monoxide exposure Hyponatremia Seizures or focal neurologic deficits are uncommon.
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DDx of HAPE
Pneumonia Asthma Pulmonary embolism Congestive heart failure Myocardial infarction CO poisoning Fever >101°F, chills, or mucopurulent sputum are typically absent
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DDx of HACE
In addition to AMS differential: Cerebrovascular accident Alcohol intoxication Brain tumor Central nervous system (CNS) infection (e.g., meningitis) Acute psychosis/delirium
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General management of altitude sickness
AMS - can monitor, rest, treat symptomatically HAPE + HACE = treat as emergency (ABCs), descent, portable hyperbaric, give O2
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Meds in altitude sickness - prevention + management - doses, and which are banned by WADA
Prevention: ibuprofen (AMS) Acetazolamide (diamox) - lowers blood pH, increasing minute ventilation + oxygenation - Banned by WADA Dexamethasone - banned Budesonide Nifedipine - Adversely affects performance but not banned, used to prevent or treat HAPE Treatment: ibuprofen, tylenol, ondansetron for sx Dexamethasone
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Prevention of altitude sickness
Graded ascent If travel to destination >2500m, spend 1 night in intermediate elevation Do not ascend >500m a day Rest day every 1000m gained High carb diet Adequate hydration Sleep hygiene at altitude More arousals, increased periodic breathing Environment should be quiet + dark, comfortable temp Avoid caffeine, nicotine, alcohol Late afternoon/ evening exercise Light bedtime snack Aggressively manage jet lag
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RF for decompression sickness
Inexperience Fatigue Hypovolemia/dehydration Poor physical conditioning Obesity PFO Atrial septal defect (ASD) Panic or anxiety while diving Rapid ascent from depth Holding breath during ascent Omitted decompression stops Flying <24hrs after diving Inadequate rest between dives
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Hx qs for decompression sickness
Get info from dive computer + buddy Details of dive (depth, time, deco stops)
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Sx of arterial gas embolism
LOC, wheezing, blood in ear, decreased reflexes, weakness or paralysis, chest pain, irregular breathing, vomiting, hemoptysis, vision changes, headache, unilateral motor changes, Gate changes, vertigo, confusion
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Physical for decompression sickness
General manifestations of gas deposition in the CNS may mimic a transient ischemic attack (TIA), cerebrovascular accident (CVA), or seizure (epilepsy): manifest by confusion, personality changes, altered level of consciousness, delirium, numbness, weakness, aphasia, paresthesias, rapidly ascending paraplegia, or paralysis. Bubble formation in the inner ear can cause tinnitus (ringing sensation), sensorineural hearing loss, and dysequilibrium, with associated nausea, vomiting, ataxia and nystagmus (the staggers). Joints may exhibit erythema and edema of periarticular surfaces, vague soreness, muscle weakness or fatigue, and pain with movement. Gas deposition in soft tissues may manifest as urticaria, mottled skin rash (cutis marmorata), or subcutaneous emphysema.
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Management of decompression sickness
100% O2 via non rebreathe mask Hyperbaric O2 chamber Echo to check for PFO once well
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Causes of tiredness in an athlete
Poor sleep, social factors, over training, and adequate carb intake, timing of carb intake, and adequate protein intake, inadequate hydration Iron deficiency, viral illness (mono), asthma, sinusitis, depression, anxiety, prescription Med, alcohol alcohol, PCOS, hypo thyroidism, diabetes, chronic fatigue syndrome, coeliac, eating disorders, malignancy, adrenal disease, renal disease, cardiac disease, HIV, hepatitis, malaria, pregnancy, postconcussion, SLE etc
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What is functional overreaching?
Increased training leading to a temporary performance reduction, with improved performance after rest. Last days two weeks, causes acute fatigue and then positive adaptation.
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What is non-functional overreaching?
Intense training leading to longer performance reduction but with full recovery after rest, accompanied by psychological or neuro endocrinological symptoms, last weeks to months
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What is overtraining syndrome?
Intense training over months leading to reduced performance, severe psych, neuro, endocrinological symptoms
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Sx + hx qs for overtraining
Decreased performance, fatigue Training Current training intensity, frequency Non training stressors Finances Relationships School Sleep Diet Menses
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Physical for overtraining
Vitals HEENT to r/o infection inc mono Neck + thyroid exam Chest auscultation Abdo exam for splenomegaly Neurological exam
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DDx for overtraining
Major depression or other psychological disorder Disordered eating pattern Organic disease (mononucleosis or other infections, hypothyroidism, anemia) Drug abuse Nutritional deficiencies Concussion
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Management of overtraining
Team approach Rest Sleep Nutrition Counselling
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Prevention of overtraining
Daily training logs Proper coaching Rest days Maximise sleep Proper nutrition
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Hx qs + sx of exercise induced bronchoconstriction
Wheezing, coughing, SOB, chest tightness Usually within 15 mins of onset of exertion Recovery within 90 mins of completion Personal or fam hx of asthma
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RF sports for exercise induced bronchoconstriction
Cold weather sports Sports w/ long duration of high intensity exercise (running, cycling, soccer, rugby)
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Physical for exercise induced bronchoconstriction
Cardiac + resp exam
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Ix for exercise induced bronchoconstriction
Gold standard is eucapnic voluntary hyperapnea testing PFTs w/ salbutamol for reversibility If neg, do pre + post exercise Inhaled mannitol testing - fall in FEV1 >15% from baseline is diagnostic
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DDx for exercise induced bronchoconstriction
Asthma with exercise exacerbation Vocal cord dysfunction (VCD) Exercise-induced hyperventilation Restrictive lung disease Cystic fibrosis Coronary artery disease Congenital/acquired heart defects Arrhythmias Congestive heart failure Cardiomyopathy GERD Anxiety
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Management + future prevention of exercise induced bronchoconstriction
Ventolin 2-4 puffs before exercise, repeat during exercise PRN If no response or needing it daily, add montelukast 10mg PO 2hrs before exercise or ICS Prevention in future Warm up Interval training with rests during to allow a refractory period Avoid triggers (cold) Breathe through nose (more humid)
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Sx of MI
CP, SOB, pre-syncope N/V
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Ix for MI
Cardiac markers, lytes, coag, CXR, ECG
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Management of MI
Support ABCs Aspirin 325mg Oxygen if low sats Nitro SL or spray - unless inferior MI IV access Morphine IV if discomfort not relieved by nitro spray Time from onset <12 hrs - reperfusion (PCI within 90 mins, fibrinolysis within 30 mins) Time from onset >12 hrs - start nitro or heparin
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ECG findings for STEMI + NSTEMI
ST elevation, new LBBB (STEMI) NSTEMI - ST depression, T wave investion
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What is HOCM?
Asymmetric LV hypertrophy Autosomal dominant Primary cause of sudden cardiac death in <35 y/o
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RF for HOCM
Fam hx of sudden cardiac death 12-30 y/o Prior hx of syncope Abnormal BP response to exercise
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Acute sx of HOCM
Collapse Brief sz like activity after collapse
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Hx qs to ask in HOCM - in clinic
Unexplained syncope Exertional chest pain or palps Dyspnea out of proportion to exertion Fam hx: sudden cardiac death, hypertrophic cardiomyopathy, Marfans
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Physical for HOCM
Usually normal exam If murmur present, usually midsystolic + heard midleft sternal border Worrisome if rising from squatting to standing or performing valsalva worsens the murmur
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Ix + ECG findings for HOCM
If genotype positive but phenotype neg, should have ECG, echo + exam annually for kids + q5yrs for adults ECG LVH findings - markedly increased voltages in precordial leads Increased voltage Repolarization abnormalities Prominent deep Q waves in left precordial leads, ischemic ST changes in 90% of cases T wave inversion, ST depression in infero-lateral leads, prominent dagger life septal Q waves in lateral leads (V4-6) and inferior leads (II, III, aVF) Echo - LVH, LV outflow obstruction Genetic testing Exercise stress testing for symptomatic pts
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DDx of SCD
Hypertrophic cardiomyopathy Dilated cardiomyopathy Congenital coronary artery anomalies arrhythmogenic right ventricular cardiomyopathy myocarditis Marfans Congenital aortic stenosis Mitral valve prolapse ion channel disorders like long QT, short Qt, Brugada, WPW, catecholaminergic polymorphic ventricular tachycardia Cocaine, amphetamines Hypo or hyperkalemia Hypo or hyperthermia Trauma (direct blow at critical time in rhythm (during ascending part of T wave) to precordium = commotio cordis) - causes VFib, most common in young boys during sports
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Management (acute + longterm) of SCD
Acute CPR AED Rapid cooling (induced hypothermia) after VF arrest Long term Implantable defib Meds - usually BB Ablation or myomectomy Disqualified from all competitive sports except low dynamic intensity
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Triggers for fatal arrhythmias during exercise
Surges in catecholamine levels Dehydration Electrolyte imbalances Increased platelet aggregation
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Evaluation of an athlete w/ condition that cause SCD
History of symptoms, particularly with exertion Family history of symptoms and sudden death. Examine ECG Echo
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What is a Osteoid Osteoma?
A small, benign, painful tumor usually affecting long bones; more common in young adults.
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What is a Osteoblastoma?
benign Similar to osteoid osteoma but larger and less painful; often found in the spine.
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What is a Enchondroma?
A benign cartilage tumor that typically occurs in the small bones of hands and feet.
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What is a Chondroblastoma?
A rare, benign cartilage tumor usually found in the ends of long bones in adolescents.
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What is a Giant Cell Tumor of Bone?
Locally aggressive but benign tumor; often arises near the knee in young adults.
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What is a Osteochondroma?
The most common benign bone tumor, often found near growth plates; it may present as a painless bony outgrowth.
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What is a Desmoid Tumor?
(Aggressive Fibromatosis): Non-metastatic but can be locally invasive; often involve deep muscles and fascia.
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What is a Giant Cell Tumor of Tendon Sheath?
A slow-growing malignant tumor, usually around the fingers or hands, that can recur locally.
215
What is a Liposarcoma?
A malignant tumor of fat tissue, which can vary in aggressiveness.
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What is a Rhabdomyosarcoma?
malignant tumor, Originates in skeletal muscle; common in children and young adults.
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What is a Leiomyosarcoma?
Arises from smooth muscle; often affects the uterus, abdomen, or blood vessels. malignant
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What is a Angiosarcoma?
A malignant tumor from blood vessels; can occur anywhere, including the skin and soft tissues.
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What is a Malignant Peripheral Nerve Sheath Tumor (MPNST)?
Often associated with neurofibromatosis type 1 (NF1); aggressive with potential for recurrence.
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What is a Fibrosarcoma?
Originates from fibrous tissue; generally affects deep tissues of limbs or trunk. malignant
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What is a Schwannomas and Neurofibromas?
benign Tumors from peripheral nerves; associated with neurofibromatosis.
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What is a Fibromas?
benign Connective tissue tumors, including fibromatosis (e.g., palmar fibromatosis or Dupuytren’s contracture).
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What is a Leiomyoma?
benign Tumors from smooth muscle; common in uterine tissue but also found in other soft tissues.
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What is a Myxoma?
benign Soft tissue tumors with a gelatinous appearance, often arising from connective tissue.
225
What is a Osteosarcoma?
malignant The most common primary bone cancer; typically occurs in the metaphysis of long bones (e.g., around the knee) in teenagers and young adults.
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What is a Chondrosarcoma?
malignant A cartilage-producing tumor; commonly found in the pelvis, femur, and shoulder, and often affects older adults.
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What is a Ewing Sarcoma?
A highly aggressive tumor seen in children and young adults; often arises in the pelvis, femur, or chest wall.
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What is Multiple Myeloma?
A cancer of plasma cells that often causes multiple lesions in bones; most common in older adults.
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What is a Lymphoma of Bone?
rare malignant tumor can appear as a primary tumor in the bone or as part of a systemic lymphoma.