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Clinical Medicine II > Exam IV Study Guide > Flashcards

Exam IV Study Guide Flashcards

1
Q

DVT

A

40-90% of all patients

Signs and symptoms
Swelling
Erythema
Pain
Homan’s sign (but not on its own)
Point tenderness in calf

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2
Q

Avascular Necrosis

A

Hip is most common joint
-Men ages 30-60 years
-*Trauma
-Long term steroid use
-RA/Lupus
-Alcoholism

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3
Q

Avascular Necrosis Symptoms

A

Antalgic gait

Pain in the groin down to medial knee

Throbbing deep hip pain

Restricted hip internal rotation, flexion, and abduction

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4
Q

Hip Osteoarthritis

A

Osteoarthritis: focal loss of articular cartilage with variable subchondral bone reaction. Joint pain and functional impairment seen.

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5
Q

Hip Osteoarthritis conservative treatments

A

Gait and balance training
Manual therapies
Systematically progressed therapeutic strengthening, flexibility and endurance, (Keeping an eye on symptoms)

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6
Q

Anterior THA

A

Access b/t sup gluteal & femoral nerves

Possibly assoc’d w/:
-Fewer dislocations
-Less time in hospital

Relatively muscle-sparing

Femur less exposed
-Could make it difficult to place hardware

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7
Q

Posterior THA

A

most common, Good femur visibility during procedure, Deep ER muscles get cut, May increase dislocation risk, May compromise sciatic nerve, No ABD muscle cuts, Preserves frontal plane gait mechanics.

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8
Q

Lateral/Direct lateral THA

A

Glut med and min reflected away from troch

Allows for better distal access if necessary

More proximal access from the entry point could risk neurovascular compromise

Again, dislocation risk lower than that for posterior approach

Frontal plane gait problems are possible

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9
Q

Greater Trochanteric Bursitis

A

Common in active patients

Bursa irritated from excessive compression/friction

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10
Q

Greater Trochanteric Bursitis treatment

A

Relieve pain and inflammation (rest, ice, NSAIDs)

Eliminate activities that make it worse

Focus on functional exercise

If truly shortened, stretching is advocated (Glutes/TFL)

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11
Q

Ischial bursitis (Weaver’s bottom)

A

Pain over the ischial tuberosity
Caused by direct pressure from prolonged sitting
Can mimic a hamstring strain
Affects thinner people and cyclists

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12
Q

Ischial bursitis (Weaver’s bottom) interventions

A

Rest, ice, NSAIDs
Injection with corticosteroids

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13
Q

Muscle strain acute phase rehab

A

1-7 days
-Initial: cold prn pain
-Avoid motions that cause pain (crutches may be used)
-Sleeping with pillows under both knees to support the injured limb
-PRICEMEM
-Painless PROM or AAROM

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14
Q

Muscle strain sub acute phase rehab

A

1-3 weeks
-Begin AROM and initiate strengthening
-Aquatic therapy to decrease weightbearing loads
-Pain free submaximal isometrics
-Pain free concentric (AROM)
-UE strengthening
-CV training- swimming with pull buoy

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15
Q

Muscle strain repair phase rehab

A

3-8 weeks
Isometric contractions at 100% without pain
No pain on full ROM
Minimal to no pain with palpation

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16
Q

muscle strain repair/function phase rehab

A

8 weeks-6 months
-Normal gait pattern without pain
-Begin fast walking
-Once ambulating 30 min at fast speed without pain, jogging can begin
-Once jogging 30 min, sprinting can begin
-Then adapt to sport/function

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17
Q

2 types of hamstring strain

A

High-speed running (biceps femoris)
-Associated with recurrence

Extensive lengthening, e.g. kick motions (proximal semimem)
-Associated with prolonged RTS

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18
Q

MCL Sprain (Grade I, II, III)

A

Mechanism = valgus force or tibiofemoral (external) torsion
Esp. w/ planted foot

Grade I = pain, but minimal tearing

Grade II = Grade I + partial macroscopic tear, swelling, ↓ ROM
-Medial capsular ligament involvement

Grade III = Grade II + complete tear; marked instability, swelling, and loss of ROM
-Possible ACL and PCL involvement

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19
Q

Grade I MCL management

A

Crutches if needed, progressive ROM & exercise as permitted by pain
RTP by 1 month

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20
Q

Grade II MCL management

A

-Crutches during acute phase
Splint or immobilizer (< 1 week)
-Progress from isometrics to full-range resistance as pain allows
-Use brace when running

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21
Q

Grade III MCL management

A

Conservative care if isolated (plan on ~ 7 weeks for return to activity)
Surgical repair more if ACL or PCL involved

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22
Q

LCL Sprain

A

Mechanism = varus force, esp. when tibia is internally rotated

Managed similarly to MCL injury, but with prolonged timeframe (~ 6 months) for conservative care

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23
Q

ACL Sprain

A

Mechanism = Noncontact with multiplanar forces (e.g. valgus collapse); other mechanisms possible

Risk factors include female gender, fatigue, various weakness, alignment, laxity, and/or joint position sense characteristics

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24
Q

ACL Injury Management

A

Conservative and surgical (repair/reconstruction) approaches are both common
-Highly dependent on patient & nature of injury

Return to activity may range 2 – 6 months

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25
Q

PCL Sprain

A

Mechanism = fall on bent knee or direct, posteriorly-oriented blow to proximal anterior tibia

Favorable outcomes with conservative management for grade I and II

If surgically repaired, patient may be immobilized in extension for 6 weeks, followed by ROM, and finally PRE at ~4 months.

26
Q

Meniscus injuries

A

medial more commonly injured than lateral, mechanisms of injury are femur-on-tibia internal rotation with planted foot and forced knee extension while tibia is rotated

Surgical resection more common than repair
-Partial meniscectomy preferred
Resistance exercise at full ROM ~ 6 weeks

27
Q

Plica

A

Plica (synovial folds) are vestiges of embryological cavities, inflamed or damaged plica may cause, catching, snapping, pain going up/down stairs.

If serious, can be resected; otherwise, rest

28
Q

Osteochondritis Dissecancs

A

Usually refers to floating piece of articular cartilage
-May involve other soft tissue like meniscus or synovium

In children, conservative care may be sufficient

In adults, surgery more likely

29
Q

Patellofemoral Pain Syndrome

A

General label describing many kinds of anterior knee/patellar pain, often associated with lateral patellar tracking, activity modification should be first approach

30
Q

Chondromalacia Patella

A

Deterioration of posterior patellar cartilage
-Progresses from swelling/softening to cartilaginous fragmentation

will lead to arthritis if not addressed

Earlier on, conservative care may work
-Activity modification, anti-inflammatories

Sometimes, surgical realignment, resurfacing, or even patellar removal will be necessary

31
Q

Patellar Subluxation/Dislocation

A

May occur as a result of forceful plant-and-twist maneuver (e.g. cutting), or direct trauma

Repeated subluxations may compromise capsule and restrict ROM

Dislocation (lateral)
-Painful
-Requires reduction followed by extension immobilization for a month

32
Q

Osgood-Schlatter

A

Tibial tubercle avulsion fracture caused by repetitive tensile stress

Usually occurs in youth and is resolved by growth of a callus

End result is a larger-than-normal tubercle

Conservative management

33
Q

Larsen-Johansson

A

Like osgood schlatter but its at the apex of the patella, conservative management

34
Q

Jumper’s Knee

A

Overuse-mediated degeneration anywhere along the patellar tendon

Early on, pain after activity

As it progresses, pain becomes more intense and/or more constant

Management involves decreasing training volume, reducing pain, and graded exercise w/ eccentric contraction modes

35
Q

Knee Osteoarthritis risk factors

A

Age
Sex
-Females @ greater risk (65+)
-Males @ greater risk before age 50
Previous knee injury
Obesity
Malalignment(s)
-Varus/valgus
-Recurvatum
-Patellar tracking
Occupation

36
Q

Knee OA idiopathic

A

There is probably a mechanism, but TBD
Possible involvement of genetics

37
Q

Knee OA post-traumatic

A

Fracture or soft tissue injury
Can include consequences of surgery (e.g. meniscectomy)

38
Q

Knee OA inflammatory

A

Pigmented villonodular synovitis
Psoriatic arthritis

39
Q

Knee OA hemophilic

A

Caused by hemarthrosis-mediated degeneration
Primary prevention is best (only) strategy, but $$$ and requires extreme vigilance
Onset may be early (20s, 30s), and often TKA will be required

40
Q

Stemmer’s Sign

A

A thickened skin fold at the base of the second toe or second finger that is a diagnostic sign for lymphedema

A positive result occurs when this tissue cannot be lifted but can only be grasped as a lump of tissue

In a negative result, it is possible to lift the tissue normally

41
Q

Complete Decongestive Therapy (CDT)

A

Manual lymphatic drainage (MLD)

Short-stretch multi-layer bandaging

Limb Clearing Exercises/HEP

5 consecutive treatment days a week for 2-6 weeks.

42
Q

Comprehensive Lymphedema Management

A

Education on basic anatomy, skin care, self-massage, self-bandaging, garment care, and infection management

Psychological and emotional support

Custom compression garments (20 mm hg-60 mm hg)

43
Q

Complete Decongestive Therapy (CDT) phase one

A

Phase One – decongestive phase (2-6 weeks)
-Mobilize edema
-Decrease volume/circumference as much as possible
-Limit fibrosclerotic tissue

44
Q

Complete Decongestive Therapy (CDT) phase two

A

self care (ongoing)
Maintain gains made in Phase One
Limit exacerbation of sx

45
Q

Manual Lymph drainage

A

a gentle, manual treatment technique consisting of several basic strokes, designed to improve the activity of intact lymph vessels by providing mild mechanical stretches on the wall, does not kneading elements and is generally applied suprafascially, whereas massage is usually applied to subfascial tissues.

46
Q

Manual lymph drainage indications

A

Edema
Swelling
Sports injuries High output failure
Arthritis
Wounds
Lymphedema
CRPS

47
Q

Combined Insufficiency

A

Combination of a high output failure and a low output failure

-High output failure due to infection, trauma or surgery
-Low output failure due to previous injury to lymph vessels or nodes, i.e. radiation therapy

48
Q

Stagnation or a blockage of lymph

A

immunoglobulins prevented from reaching the sites where they can perform their immune functions

49
Q

Kinmonth syndrome

A

inguinal lymph node fibrosis

50
Q

Primary lymphedema: Milroy disease

A

observed at birth due to gene mutation- RARE

51
Q

Primary lymphedema: Lymphedema Praecox

A

developed before 35 y/o

52
Q

Primary lymphedema: Lymphedema Tarda

A

developed after age 35

53
Q

Symptoms of Lymphedema

A

Tightness/heaviness/discomfort in the area

Not usually painful

Swelling and decrease in skin mobility

Loss of strength or flexibility in a limb

Variations in skin temperature and/or color

54
Q

Lipedema

A

Painful “Fluid in the fat” disorder
Feet are not involved

55
Q

Stewart-Treves syndrome

A

Rare angiosarcoma that develops in people with long-standing lymphedema.

Usually people have a hx of breast CA that was treated with radical mastectomy.

56
Q

Stage 0 or Latent lymphedema

A

lymph transport is impaired, but there is no clinical evidence of swelling. May last months or years.

57
Q

Stage I lymphedema

A

chronic inflammatory response to the excessive protein in the interstitium
pitting on pressure
reverses with elevation
Subcutaneous tissues begin to fibrose due to protein buildup, progressing the lymphedema from Stage I to II.

58
Q

Stage II lymphedema

A

Non-pitting
Does not reduce on elevation of the limb
Clinical fibrosis is present- skin is thick and rigid
Clear, sticky lymph fluid may ooze from pores
Chronic inflammation can lead to recurrent bacterial and fungal infections

59
Q

Stage III lymphedema/ lymphostatic elephantiasis

A

severe non-pitting
Large lobular folds
fibrotic edema with atrophic skin changes such as thickened, leathery, keratotic skin, skin folds with tissue flaps, papillomas (warty like overgrowth)

60
Q

Functional Severity: Minimal

A

less than 3cm difference between limbs
Less than 20% increase in limb volume

61
Q

Functional Severity: Moderate

A

3-5 cm difference
20-40% increase in volume

62
Q

Functional Severity: Severe

A

> 5 cm difference AND a positive Stemmers sign
40% increase in volume

Clinical Medicine II (5 decks)

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