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CASEM > High Yield 5 > Flashcards

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?

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 is most effective if used early.
Joint mobilization, progressive weight-bearing, strengthening, and return to daily activities are important aspects of care directed by physical therapy.
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

Ix for OA

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

Focal idiopathic alteration of subchondral bone with risk for instability and disruption of adjacent articular cartilage that may result in premature osteoarthritis

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19
Q

What are the common places osteochondritis dissecans affects?

A

Posterolateral aspect of medial femoral condyle, talar dome, and humeral capitellum but can occur in all large joints

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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
Q

Management + RTP of osteochondritis dissecans

A

If asymptomatic, incidental finding = monitor until radiographic healing

Stable lesion
non wt bearing 6-8 wks
If no improvement at 6mo, refer for surgery

Unstable lesion
refer to ortho for possible fixation of loosened fragment
Debridement, fixation, drilling, allograft
Refer all adults to ortho

RTP
3-4mo
Complications

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26
Q

DDx for hypermobility

A

Ehlers-Danlos syndrome classic type
Marfan syndrome
Loeys-Dietz syndrome
Ankylosing spondylitis
Rheumatoid arthritis
Fibromyalgia
Multiple sclerosis
Amyotrophic lateral sclerosis
Autonomic polyneuropathies
Myopathy
Chronic fatigue syndrome
Osteogenesis imperfecta

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27
Q

Management of hypermobility

A

PT
OT
Splints, orthotics

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28
Q

RF for hypermobility

A

Females
Children + teens

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29
Q

Conditions associated w/ hypermobility

A

Recurrent joint subluxation and dislocation
Pes planus
Chronic pain
Anxiety and depression
Gastroesophageal reflux disease (GERD)
Irritable bowel syndrome (IBS)
Syncope
Orthostatic hypotension

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30
Q

What is osteoporosis?

A

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

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31
Q

What is osteopenia vs osteoporosis?

A

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

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32
Q

Types of osteoporosis

A

Primary: age-related (postmenopausal estrogen deficiency, age-related vitamin D deficiency)
Secondary: (drug or concurrent medical condition etiology)

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33
Q

Hx + Ix for osteoporosis

A

Hx
Low trauma #
Height loss

Investigations
DEXA
T + L spine to evaluate for #

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34
Q

Management of osteoporosis

A

Bisphosphonates
Inhibit osteoblast + osteoclast activity
SE: N/V, abdo pain, esophagitis, osteonecrosis of jaw

Selective estrogen receptor modulators (raloxifene)
PTH (forteo)
Calcitonin
Denosumab
Exercise + balance therapy
Repeat BMD q2yrs

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35
Q

Prevention of osteoporosis

A

Identify + treat secondary causes
Vit D + calcium supplement

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36
Q

RF for osteoporosis

A

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

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37
Q

What is myofascial pain syndrome?

A

Myofascial trigger points are “knots” in muscle that cause pain
MPS is >1 MTP

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38
Q

Sx + physical for myofascial pain syndrome

A

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

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39
Q

RF for myofascial pain syndrome

A

Poor posture
Overuse
Repetitive motion
Deconditioned muscle
Prolonged sitting

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40
Q

Management of myofascial pain syndrome

A

Address biomechanical factors
Dry needling, trigger point inj, acupuncture

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41
Q

Sx + physical exam for fibromyalgia

A

Sx
Widespread, symmetrical pain
Poor sleep, fatigue
Associated w/ myofascial pain

Exam
Tenderness in multiple soft tissue locations

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42
Q

What is a stress #?

A

Damage d/t repetitive loading that exceeds healing capacity
Can range from mild periosteal reaction to displaced #

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43
Q

What are low vs high risk stress #?

A

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

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44
Q

RF for stress #

A

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)

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45
Q

Sx of stress #

A

Insidious pain w/ repetitive activity
Pain at rest
Ask about RF, nutrition, steroid use, menses

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46
Q

Physical for stress #

A

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

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47
Q

Ix for stress #

A

XR, repeat in 2-3 wks if normal
Lucency or callus formation visible

Bone scan
MRI is gold standard
Labs: 25-OH vitamin D3, complete blood count (CBC), chem 7, calcium, thyroid-stimulating hormone (TSH), albumin, prealbumin, phosphate, and parathyroid hormone
Females with menstrual dysfunction: follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, testosterone, human chorionic gonadotropin (HCG)
Dexamethasone suppression test if excess cortisol suspected

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48
Q

DDx for stress #

A

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.

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49
Q

Management of stress # (general)

A

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

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50
Q

Complications of stress #

A

Complete fracture, delayed union, nonunion, avascular necrosis

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51
Q

Prevention of stress #

A

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).

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52
Q

Sport that causes stress fracture of coracoid process

A

Trapshooting

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53
Q

Sport that causes stress fracture of Scapula

A

Running with hand weights

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54
Q

Sport that causes stress fracture of humerus

A

Throwing, racket sports

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55
Q

Sport that causes stress fracture of olecranon

A

Throwing, pitching

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56
Q

Sport that causes stress fracture of ulna

A

Racket sports, gymnastics, volleyball, swimming, wheelchair sports

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57
Q

Sport that causes stress fracture of Pars interarticularis

A

Gymnastics, ballet, cricket fast bowling, volleyball, spring board diving

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58
Q

Sport that causes stress fracture of Pubic ramus, femur

A

Distance running, ballet

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59
Q

Sport that causes stress fracture of Tibia

A

Running

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60
Q

Sport that causes stress fracture of fibula

A

Running, ballet, aerobics

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61
Q

Sport that causes stress fracture of Medial malleolus

A

Running, basketball

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62
Q

Sport that causes stress fracture of talus

A

Pole vaulting

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63
Q

Sport that causes stress fracture of navicular

A

Sprinting, mid distance running, handling, long jump, triple jump, football

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64
Q

Sport that causes stress fracture of base of second metatarsal

A

Ballet

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65
Q

Sport that causes stress fracture of 5th metatarsal

A

Tennis, ballet

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66
Q

Sport that causes stress fracture of Sesamoid bone

A

Running, ballet, basketball, skating

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67
Q

Management of femoral neck stress fracture

A

Bed rest for one week then gradual weight-bearing if non-displaced, if displaced needs surgical fixation

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68
Q

Management of anterior tibia fracture

A

Non-weightbearing on crutches for six weeks or screw fixation

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69
Q

Management of medial malleolus stress fracture

A

Non-wt bearing cast immobilisation for six weeks or surgical fixation

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70
Q

Management of talus stress fracture

A

Non-wt bearing cast immobilisation for six weeks or surgical fixation

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71
Q

Management of navicular stress fracture

A

Non-weight bearing cast immobilisation for six weeks or surgical fixation

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72
Q

Management of base of 5th metatarsal stress fracture

A

Cast immobilisation

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73
Q

Management of base of 2nd metatarsal stress fracture

A

Non-wt bearing x2 wks then partial wt bearing x2 wks

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74
Q

Management of sesamoid stress fracture

A

Non wt bearing x4 wks

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75
Q

What is myositis ossificans?

A

A localized, nonneoplastic, 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.

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76
Q

RF for myositis ossificans

A

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

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77
Q

Sx of myositis ossificans

A

Pain, stiffness, weakness, decreased muscle mass
Night pain
Signs of MO present 2-3wks post injury - presents as unresponsive to treatment

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78
Q

Physical for myositis ossificans

A

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

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79
Q

Ix for myositis ossificans

A

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

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80
Q

DDx for myositis ossificans

A

Muscle contusion
Muscle or tendon tear
Fracture
Malignant neoplasm: osteosarcoma, lymphoma, or rhabdomyosarcoma
Compartment syndrome
Abscess
Rhabdomyolysis

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81
Q

Management of myositis ossificans

A

Self limiting
RICE
Non painful passive stretching + strengthening
Shock wave therapy
RTP usually 3-6mo
Sx can persist for >1yr

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82
Q

Prevention of myositis ossificans when contusion occurs

A

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

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83
Q

Where do mets come from?

A

Lung, breast, prostate ϲaոϲеr, and multiple myеlοma

84
Q

What imaging to use for ?lytic lesion?

A

Bone scan
In multiple myeloma, whole body MRI often used

85
Q

Types of Benign tumors

A

Osteoid Osteoma: A small, painful tumor usually affecting long bones; more common in young adults.
Osteoblastoma: Similar to osteoid osteoma but larger and less painful; often found in the spine.
Enchondroma: A cartilage tumor that typically occurs in the small bones of hands and feet.
Chondroblastoma: A rare, benign cartilage tumor usually found in the ends of long bones in adolescents.
Giant Cell Tumor of Bone: Locally aggressive; often arises near the knee in young adults.
Osteochondroma: The most common benign bone tumor, often found near growth plates; it may present as a painless bony outgrowth.
Fibrous Dysplasia: A benign fibro-osseous lesion where normal bone is replaced with fibrous tissue.
Aneurysmal Bone Cyst: A blood-filled, expanding cystic lesion that can cause pain and swelling.

86
Q

Types of malignant tumors

A

Osteosarcoma: The most common primary bone cancer; typically occurs in the metaphysis of long bones (e.g., around the knee) in teenagers and young adults.
Chondrosarcoma: A cartilage-producing tumor; commonly found in the pelvis, femur, and shoulder, and often affects older adults.
Ewing Sarcoma: A highly aggressive tumor seen in children and young adults; often arises in the pelvis, femur, or chest wall.
Malignant Fibrous Histiocytoma of Bone: A rare tumor similar to osteosarcoma; can affect any bone, usually in adults.
Fibrosarcoma of Bone: Rare and similar to malignant fibrous histiocytoma; usually found in long bones.
Multiple Myeloma: A cancer of plasma cells that often causes multiple lesions in bones; most common in older adults.
Lymphoma of Bone: Rare; can appear as a primary tumor in the bone or as part of a systemic lymphoma.
Metastatic Bone Disease: Secondary bone tumors originating from cancers such as breast, lung, prostate, and kidney cancer; common in adults.

87
Q

Types of benign soft tissue tumors

A

Lipomas: Tumors from fat cells; common and often painless.
Hemangiomas: Tumors from blood vessels; often found in infants.
Schwannomas and Neurofibromas: Tumors from peripheral nerves; associated with neurofibromatosis.
Fibromas: Connective tissue tumors, including fibromatosis (e.g., palmar fibromatosis or Dupuytren’s contracture).
Leiomyomas: Tumors from smooth muscle; common in uterine tissue but also found in other soft tissues.
Myxomas: Soft tissue tumors with a gelatinous appearance, often arising from connective tissue.

88
Q

types of malignant soft tissue tumor

A

Desmoid Tumors (Aggressive Fibromatosis): Non-metastatic but can be locally invasive; often involve deep muscles and fascia.
Giant Cell Tumor of Tendon Sheath: A slow-growing tumor, usually around the fingers or hands, that can recur locally.
Pigmented Villonodular Synovitis (PVNS): Affects the joint lining, particularly in the knee; can be locally invasive.
Liposarcoma: A malignant tumor of fat tissue, which can vary in aggressiveness.
Rhabdomyosarcoma: Originates in skeletal muscle; common in children and young adults.
Leiomyosarcoma: Arises from smooth muscle; often affects the uterus, abdomen, or blood vessels.
Synovial Sarcoma: Often occurs near joints, especially in young adults.
Angiosarcoma: A malignant tumor from blood vessels; can occur anywhere, including the skin and soft tissues.
Malignant Peripheral Nerve Sheath Tumor (MPNST): Often associated with neurofibromatosis type 1 (NF1); aggressive with potential for recurrence.
Fibrosarcoma: Originates from fibrous tissue; generally affects deep tissues of limbs or trunk.
Epithelioid Sarcoma: Rare; can mimic benign conditions but is often aggressive.
Undifferentiated Pleomorphic Sarcoma (UPS): Previously called “malignant fibrous histiocytoma,” a high-grade tumor without clear differentiation.

89
Q

What is gout?

A

Inflammatory deposition of monosodium urate crystals

90
Q

Stages of gout

A

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
Q

Common joints affected by gout

A

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
Q

RF for gout

A

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
Q

Sx + physical for gout + signs of tophi

A

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
Q

Ix for gout

A

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
Q

DDx for gout

A

Pseudogout
Rheumatoid arthritis
Septic arthritis
Osteoarthritis
Reactive arthritis
Osteomyelitis
Malignancy
Joint trauma

96
Q

Management of gout

A

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
Q

Prevention of gout

A

Minimize alcohol
Minimize meat + seafood
Increase dairy
Minimize diuretic use
Urate lowering meds

98
Q

Indications for preventative meds in gout, + when to start

A

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
Q

What is pseudogout?

A

Calcium pyrophosphate deposition disease (CPPD)

100
Q

RF for pseudogout

A

Gout (20% may be hyperuricemic)
Hemochromatosis
Hypothyroidism
Trauma
Osteoarthritis
Hyperparathyroidism
Hemosiderosis
Hypophosphatasia
Hypomagnesemia
Aging
Amyloidosis

101
Q

Sx of pseudogout

A

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
Q

Physical for pseudogout

A

Warmth
Edema/effusion
Tender
Limited range of motion

103
Q

Ix for pseudogout

A

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
Q

DDx for pseudogout

A

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
Q

Management of pseudogout

A

Joint aspiration
Intra-articular steroid inj
Joint rest, splinting
NSAIDs
Colchicine 2nd line

106
Q

Prevention of pseudogout

A

Colchicine 0.6mg BID for recurrent attacks

107
Q

Sx + hx qs for rheumatoid arthritis

A

​​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
Q

RF for rheumatoid arthritis

A

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
Q

Physical for rheumatoid arthritis

A

​​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
Q

Ix for rheumatoid arthritis

A

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
Q

DDx for rheumatoid arthritis

A

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
Q

Management of rheumatoid arthritis

A

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
Q

Complications of rheumatoid arthritis

A

Increased risk of CV disease + stroke
Increased risk of infection
Increased risk of lymphoma

114
Q

What features suggest an inflammatory disorder?

A

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
Q

Differential diagnosis for atraumatic single swollen joint

A

Septic arthritis, gout, pseudo gout, Lyme disease, reactive or psoriatic arthritis, osteoarthritis, malignancy (synovial sarcoma), rheumatoid arthritis, sarcoidosis, haemophilia

116
Q

Differential diagnosis for atraumatic polyarthritis (pain + swelling)

A

Rheumatoid arthritis, viral arthritis (EBV, parvo virus), psoriatic or reactive arthritis, inflammatory osteoarthritis, SLE, rheumatic fever, haemachromatosis, Sjögren’s syndrome

117
Q

Differential diagnosis for polyarthralgia (joint pain without swelling)

A

Drug induced (quinolones, acyclovir, vitamin A, beta blockers, statins)
Viral infection, thyroid disease, parathyroid disease, PMR, inflammatory myositis, leukaemia, depression, somatisation, fibromyalgia

118
Q

What is the work up for Lyme disease?

A

Enzyme immunoassay and Western blot.

119
Q

Hx qs for syncope

A

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

120
Q

Physical on sideline for syncope

A

Check BP both arms
Consider rectal temp
Full neuro eval
Glucose

121
Q

Physical in office for syncope

A

Orthostatic vitals
Cardiac exam - standing, supine + supine w/ valsalva
Neuro exam

122
Q

Ix for syncope

A

ECG
Labs - CBC, TSH, glucose
Echo
Holter
Stress testing

123
Q

DDx for syncope

A

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

124
Q

Prevention of syncope

A

Education regarding warm up + cool down
Proper nutrition + hydration
Appropriate clothing

125
Q

What is rhabdomyolysis?

A

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

126
Q

RF for rhabdomyolysis

A

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

127
Q

Sx of rhabdomyolysis

A

Muscle pain, weakness, dark urine
Fever, tachycardia, nausea
Malaise

128
Q

Physical for rhabdomyolysis

A

Muscle tenderness, swelling, weakness
Hypovolemic state
Decreased urine output

129
Q

Ix for rhabdomyolysis (initially + once resolved)

A

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

130
Q

DDx for rhabdomyolysis

A

Muscle strain
Delayed onset muscle soreness
Muscle infection
Sickle cell crisis
Nontraumatic myopathies
Hypercalcemia/hyperparathyroidism
Hypo/hyperthyroidism

131
Q

Management of rhabdomyolysis

A

Aggressive fluid resus w/ isotonic saline
Bicarb administration
Treat underlying cause

132
Q

Complications (early + late) of rhabdomyolysis

A

Early complications:
Hyperkalemia
Hypocalcemia
Cardiac arrhythmia
Cardiac arrest
Compartment syndrome

Late complications (past 12 hr):
ARF with oliguria
Hypercalcemia
Disseminated intravascular coagulation
Compartment syndrome

133
Q

Sx of hypoglycemia + glucose reading

A

Sweating, HA, tremor, hunger, altered LOC
<3.6

134
Q

Management of hypoglycemia

A

glucose gel in buccal mucosa or glucagon 1mg IM
If sx resolve w/ glucagon, give long acting carb and monitor glucose frequently

135
Q

Prevention of hypoglycemia w/ exercise

A

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

136
Q

What is REDS?

A

Dietary intake is insufficient for energy expenditure (problematic low energy availability)

137
Q

Hx qs to ask for REDS

A

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

138
Q

Physical for REDS

A

Ht, wt, BMI
Orthostatic vitals
Hair, skin, nails
Thyroid exam
Cardiac exam
Consider pelvic exam if amenorrhea

139
Q

Ix for REDS

A

Labs - CBC, lytes, iron, TSH, LH + FSH (low or normal), estrogen (low), prolactin (normal), cortisol (mildly elevated)
PT
DEXA if stress #

140
Q

DDx for REDS

A

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

141
Q

RF for REDS

A

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

142
Q

Management of REDS

A

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

143
Q

Complications of REDS

A

Infertility
Decreased BMD
Iron deficiency
Increased risk of illness + injury
Stress #
Depression + anxiety
Decreased strength + endurance
Decreased concentration + coordinati

144
Q

Prevention of REDS

A

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

145
Q

What qs to ask in infertility/ abnormal menses?

A

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

146
Q

Physical for infertility/ abnormal menses

A

BP, HR
Ht, wt, body fat %
Skin + hair
Thyroid exam
Pelvic exam

147
Q

Ix for infertility/ abnormal menses

A

bHCG
TSH, T4
FSH, LH
Prolactin, total + free testosterone, estrogen
Pelvic US
Head MRI for ?pituitary tumor
Male factors

148
Q

DDx for infertility/ abnormal menses

A

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

149
Q

Management of infertility

A

Chart cycle, intercourse, training
Functional hypothalamic amenorrhea
Reduce training
Increase body wt
Calcium + vit D

150
Q

What is oligomenorrhea?

A

Menstrual cycles >35 days, no perceptible s

151
Q

What is amenorrhea?

A

No menstrual cycle >3mo

152
Q

What is primary amenorrhea?

A

> 15 y/o no periodW

153
Q

What is PARmed-X?

A

screening tool to identify high risk pregnancy (prior spontaneous abortion, placenta previa, spotting, incompetent cervix, triplets, medical conditions)
provides prescription exercise program in pregnancy

154
Q

What advice can you give for exercise during pregnancy?

A

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

155
Q

What are Warning signs to stop exercise in pregnancy?

A

Vaginal bleeding
Dyspnea prior to exertion
Dizziness
Headache
Chest pain
Muscle weakness
Calf pain or swelling
Preterm labor
Decreased fetal movements
Amniotic fluid leakage

156
Q

What are Absolute CI to exercise in pregnancy?

A

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

157
Q

What are common MSK issues in pregnancy?

A

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

158
Q

What are the best forms of exercise during pregnancy?

A

Swimming
Stationary cycling
Weight training
Walking

159
Q

Positive effects of exercise during pregnancy

A

potential risk reduction for development of GDM, pregnancy-induced HTN, and preeclampsia
a decrease in postpartum depression symptoms
decreased incidence of urinary incontinence

160
Q

Sx of altitude sickness + onset

A

usually onset within 12-24hrs and self limited
Nausea
Light-headedness
Headache
Insomnia
Anorexia
Malaise
Fatigue
Weakness
Impaired memory
Inability to focus or concentrate

161
Q

Sx of HAPE

A

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

162
Q

Sx of HACE

A

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

163
Q

RF for altitude sickness

A

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

164
Q

Signs of AMS on exam

A

usually normal, potentially tachy or bradycardic

165
Q

Signs of HAPE on exam

A

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

166
Q

Signs of HACE on exam

A

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

167
Q

DDx of AMS

A

Dehydration
Exhaustion
Viral syndrome
Gastroenteritis
Hangover
Hypothermia
Carbon monoxide exposure
Hyponatremia
Seizures or focal neurologic deficits are uncommon.

168
Q

DDx of HAPE

A

Pneumonia
Asthma
Pulmonary embolism
Congestive heart failure
Myocardial infarction
Fever >101°F, chills, or mucopurulent sputum are typically absent

169
Q

DDx of HACE

A

In addition to AMS differential:
Cerebrovascular accident
Alcohol intoxication
Brain tumor
Central nervous system (CNS) infection (e.g., meningitis)
Acute psychosis/delirium

170
Q

General management of altitude sickness

A

Descent to a lower altitude is the mainstay of treatment for any HAI.
Low-intensity descent of at least 500 m is recommended.
Avoid further ascent until symptoms resolve.
Supplemental oxygen 2 to 4 L/min if available
Portable hyperbaric if unable to descend

171
Q

Meds in altitude sickness - prevention + management - doses, and which are banned by WADA

A

Oral acetaminophen 650 to 1,000 mg or ibuprofen 600 mg for pain or headache; ondansetron orally disintegrating tablet (ODT) 4 mg PO q4–6h for nausea and vomiting

Acetazolamide (diamox) - lowers blood pH, increasing minute ventilation + oxygenation
Banned by WADA
125mg PO BID - start day before ascent
SE: nausea, tingling, altered taste, dizzy, HA

Ibuprofen
600mg PO TID for AMS prevention

Dexamethasone
Banned by WADA
Reduces risk of AMS + HAPE
Prevention: 4mg PO BID - start day before ascent, continue for first 2 days at altitude
Treatment of HAPE: 4mg PO QID
Treatment of HACE: 8mg loading dose then 4mg PO QID

Budesonide
200ug inhaled BID starting 3 days prior to ascent
Prevents AMS

Nifedipine
Adversely affects performance but not banned
Used to prevent or treat HAPE
30mg ER PO BID

172
Q

Prevention of altitude sickness

A

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

173
Q

RF for decompression sickness

A

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

174
Q

Hx qs for decompression sickness

A

Get info from dive computer + buddy
Details of dive (depth, time, deco stops)

175
Q

Sx of arterial gas embolism

A

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

176
Q

Physical for decompression sickness

A

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.

177
Q

Management of decompression sickness

A

100% O2 via non rebreathe mask
Hyperbaric O2 chamber
Echo to check for PFO once well

178
Q

Causes of tiredness in an athlete

A

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

179
Q

What is functional overreaching?

A

Increased training leading to a temporary performance reduction, with improved performance after rest. Last days two weeks, causes acute fatigue and then positive adaptation.

180
Q

What is non-functional overreaching?

A

Intense training leading to longer performance reduction but with full recovery after rest, accompanied by psychological or neuro endocrinological symptoms, last weeks to months

181
Q

What is overtraining syndrome?

A

Intense training over months leading to reduced performance, severe psych, neuro, endocrinological symptoms

182
Q

Sx + hx qs for overtraining

A

Decreased performance, fatigue
Training
Current training intensity, frequency
Non training stressors
Finances
Relationships
School
Sleep
Diet
Menses

183
Q

Physical for overtraining

A

Vitals
HEENT to r/o infection inc mono
Neck + thyroid exam
Chest auscultation
Abdo exam for splenomegaly
Neurological exam

184
Q

DDx for overtraining

A

Major depression or other psychological disorder
Disordered eating pattern
Organic disease (mononucleosis or other infections, hypothyroidism, anemia)
Drug abuse
Nutritional deficiencies
Concussion

185
Q

Management of overtraining

A

Team approach
Rest
Sleep
Nutrition
Counselling

186
Q

Prevention of overtraining

A

Daily training logs
Proper coaching
Rest days
Maximise sleep
Proper nutrition

187
Q

Hx qs + sx of exercise induced bronchoconstriction

A

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

188
Q

RF for exercise induced bronchoconstriction

A

Cold weather sports
Sports w/ long duration of high intensity exercise (running, cycling, soccer, rugby)

189
Q

Physical for exercise induced bronchoconstriction

A

Cardiac + resp exam

190
Q

Ix for exercise induced bronchoconstriction

A

PFTs w/ salbutamol for reversibility
If neg, do pre + post exercise
Inhaled mannitol testing - fall in FEV1 >15% from baseline is diagnostic

191
Q

DDx for exercise induced bronchoconstriction

A

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

192
Q

Management + future prevention of exercise induced bronchoconstriction

A

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
Avoid triggers (cold)
Breathe through nose (more humid)

193
Q

Sx of MI

A

CP, SOB, pre-syncope
N/V

194
Q

Ix for MI

A

Cardiac markers, lytes, coag, CXR, ECG

195
Q

Management of MI

A

Brief hx + physical
Review fibrinolytic checklist
Check CI
Support ABCs
Aspirin 325mg
Oxygen if needed
Nitro SL or spray
IV access
Morphine IV if discomfort not relieved by nitro spray

196
Q

ECG findings for STEMI + NSTEMI

A

ST elevation, new LBBB (STEMI)
Time from onset <12 hrs - reperfusion (PCI within 90 mins, fibrinolysis within 30 mins)
Time from onset >12 hrs - start nitro or heparin

NSTEMI - ST depression, T wave investion

197
Q

What is HOCM?

A

Asymmetric LV hypertrophy
Autosomal dominant
Primary cause of sudden cardiac death in <35 y/o

198
Q

RF for HOCM

A

Fam hx of sudden cardiac death
12-30 y/o
Prior hx of syncope
Abnormal BP response to exercise

199
Q

Acute sx of HOCM

A

Collapse
Brief sz like activity after collapse

200
Q

Hx qs to ask in HOCM - in clinic

A

Unexplained syncope
Exertional chest pain or palps
Dyspnea out of proportion to exertion
Fam hx: sudden cardiac death, hypertrophic cardiomyopathy, Marfans

201
Q

Physical for HOCM

A

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

202
Q

Ix + ECG findings for HOCM

A

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

203
Q

DDx of SCD

A

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

204
Q

Management (acute + longterm) of SCD

A

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

205
Q

Triggers for fatal arrhythmias during exercise

A

Surges in catecholamine levels
Dehydration
Electrolyte imbalances
Increased platelet aggregation

206
Q

Evaluation of an athlete w/ condition that cause SCD

A

History of symptoms, particularly with exertion
Family history of symptoms and sudden death.
Examine
ECG
Echo

CASEM (13 decks)

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