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Clin Med II - FINAL > Pathologies Related To The Knee > Flashcards

Pathologies Related To The Knee Flashcards

1
Q

What is deep vein thrombosis?

A
  • partial or complete occlusion of a vein by a clot
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2
Q

What are risk factors for DVT?

A

Conditions involving at least 2 of the following:
- venous stasis
- hypercoagulability
- damage to the venous wall

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3
Q

What is the etiology of DVT?

A
  • 50% unknown
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4
Q

What are some possible contributors to DVT?

A
  • Prior DVT
  • Hx of cancer, CHF, or lupus
  • Recent and major infection, surgery, or trauma
  • Present chemotherapy, immobility, or pregnancy
  • Use of oral contraceptives or hormone therapy
  • Clotting disorder
  • > 60 yrs. of age
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5
Q

DVT is the __ most common cardiovascular disease

A

3rd

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6
Q

Where is DVT most common?

A

in LE deep veins (90%)

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7
Q

Why should we be concerned with a DVT after a total joint replacement?

A
  • MOST common cause of readmissions and death after TKA/THA
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8
Q

What should we know about hospital related deaths from DVT?

A

PREVENTABLE

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9
Q

What is the pathogenesis of DVT?

A
  • Greater exposure of platelets and clotting factors to damaged venous wall
  • Fibrin, leukocytes, and erythrocytes adhere and form thrombus
  • Basically, the reparative process goes bad
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10
Q

What can be done to treat DVTs?

A
  • Early and regular exercise
    > As prevention for sure
    > May need to wait on anticoagulant therapy to take effect to avoid a PE from motion with treatment
  • Anticoagulants
  • Compression stockings
  • Intermittent Pneumatic Compression devices
  • Avoid SAD
  • Eliminate persistent smoking and drinking
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11
Q

What will we find in a pt’s history with DVT?

A

Hx including:
* ~50% asymptomatic in early stages
* Typically, gradual onset of dull ache, tightness, and P! in the calf with prior mentioned risk factors

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12
Q

What is included in the CDR for DVTs?

A
  • Edema: Likely pitting (70% of patients)
  • Increased calf girth
  • Calf pain and tenderness
    50% of patients
  • Worsened with walking and possibly with dependent positions
  • Less and less relief with rest and elevation as condition worsens
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13
Q

What will we find with palpation with DVT?

A

possible redness and warmth

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14
Q

What is the referral with DVT?

A
  • per CDR:
  • urgent if ≤ 17% probability of DVT with ≤ 2
  • emergency if 75% probability of DVT with ≤ 3
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15
Q

What can a DVT lead to?

A

Pulmonary Embolism

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16
Q

What is a pulmonary embolism?

A

Pathogenesis- DVT that moves and lodges into smaller artery supplying the lungs

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17
Q

What should we know about clinical manifestations of a PE?

A

Often non-specific… “the great masqueraders”

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18
Q

What are the MOST common S&S of a PE?

A

SOB, wheezing, and/or rapid breathing may be the only symptom
> Pleuritic chest P! (T2-4 shared innervation)- sudden, sharp and stabbing chest P! possibly exacerbated by:
* Deep inspiration
* Coughing
* Mechanical pain may occur due to lung fascia attaching to ribs and thoracic vertebra
* Trunk motion
* UE motion
* Thoracic and rib accessory motion testing

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19
Q

What are some other clinical manifestations of a PE that are potentially less common?

A
  • Bloody cough
  • P!ful breathing at rest
  • Fainting
  • Tachycardia and palpitations
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20
Q

What is the referral with a PE?

A

Urgent if < 2/6
Emergency if ≥ 2/6

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21
Q

What is a part of the CDR with a PE?

A
  • Clinical S&S of DVT (i.e., LE swelling; TTP along deep veins; pitting edema; collateral and NOT varicose veins
  • HR > 100 bpm
  • Immobilization/Sx in prior 4 wks.
  • Prior DVT/PE
  • Bloody cough
  • Malignancy or cancer Rx in last 6 mths.
  • Alternative dx is LESS likely than PE
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22
Q

What is peripheral arterial disease?

A

ischemia leading to symptoms in the MOST distal area from the blocked a.

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23
Q

Where is PAD most often?

A

in LEs and in calf

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24
Q

What are some risk factors/etiologies for PAD?

A
  • ≥ 45 yrs. of age
  • Family hx of MI or sudden cardiac death before 55 yrs.
  • Recent or current smoker
  • Physical inactivity
  • Metabolic syndrome
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25
Q

What is the pathogenesis of PAD?

A

Atherosclerosis or plaque build up in aa that also promotes vascular constriction thus further limiting circulation

26
Q

When do symptoms begin with PAD?

A

once 50% of a. is narrowed

27
Q

What are some clinical manifestations and S&S of PAD?

A

Intermittent claudication
* LE P!, MOST often the calf, with walking and elevated positions
* Unilateral or bilateral
* Often described as cramping but also may be weakness, pressure, or aching
* Relieved with rest and dependent position

28
Q

What will we find distal to the ischemic area with PAD?

A
  • Loss of pulses
  • TTP
  • Muscle atrophy and weakness
  • Loss of hair
  • Cool and bluish skin
  • Bruit on auscultation
  • Possible necrosis/wound
29
Q

What can happen in the presence of SEVERE ischemia?

A

the P! may also occur at rest and create sleep interruptions

30
Q

How do we test for ankle brachial index (ABI) with PAD?

A

IN SUPINE
- Assess posterior Tibial/Brachial SYSTOLIC BP in all 4 extremities
- Divide ankle by brachial pressure

31
Q

What makes the ABI invalid?

A

hx of HTN

32
Q

What is an abnormal finding with ABI?

A
  • < .9 (the lower the worse the dz)- LR+ = 1.6-7.6; LR- = .0-.86
  • ≥ 1.4 (aa. unable to be compressed vv. due excessive hardening from atherosclerosis)
33
Q

How could you differentiate calf pain due to PAD vs stenosis?

A
  • symptoms (thorough hx)
  • Lumbar stenosis with Bicycle Test
  • DVT which is more P!ful in a dependent position and relieved with elevation
34
Q

What kind of referral is PAD?

A

Urgent referral to vascular MD

35
Q

What is osteochondritis dissecans?

A

changes to subchondral bone

36
Q

Is osteochondritis dissecans common?

A

no RARE

37
Q

What population/body part is osteochondritis dissecans MOST common in?

A

… younger biological boys through early adulthood
… in medial Femoral condyle and Talus

38
Q

What is the etiology of osteochondritis dissecans?

A
  • MOSTLY unknown
  • Joint rotational or shearing trauma, like a sprain
39
Q

What are the pathomechanics and pathogenesis of osteochondritis dissecans?

A
  • Fracture to subchondral bone involving cortical plate and cancellous bone
  • Possible ischemia (AVN) then separation of subchondral bone from convex weightbearing end of bones
  • Overlying articular cartilage can remain viable
40
Q

What are the clinical manifestations and S&S of osteochondritis dissecans?

A
  • Persistent pain, not progressing as expected
  • May progress into severe pain if fragment displaces with joint locking, catching, and swelling
  • S&S of hypermobility/instability of involved ligament but with persistent age-related joint-like changes
41
Q

What will we find in our scan with osteochondritis dissecans?

A
  • ROM- limited and painful, particularly with ext
  • Resisted/MMT- may be weak and painful, particularly at end range ext
  • Compression likely (+) and distraction relieving
42
Q

What will we find in our biomechanical exam with osteochondritis dissecans?

A
  • Stability tests (+) for specific ligament(s)
  • TTP over femoral condyle
43
Q

What kind of referral is osteochondritis dissecans?

A

Urgent referral to MD

44
Q

What is osteochondritis dissecans BEST imaged by?

A

MRI

45
Q

Why couold it take up to 2-3 years to revascularize and heal with osteochondritis dissecans?

A

May take up to 2-3 years to revascularize and heal if the following joint stresses are present:
- Higher BMI
- Deficient passive restraints
- M. imbalances
- Impaired proprioception

46
Q

What is protection to avoid separation of subchondral bone and articular cartilage into the joint also called?

A

joint mouse

47
Q

Why is a joint mouse common at the knee?

A

loss of joint surface congruancy

48
Q

What should we treat non-operative stable lesions like?

A

Rx as joint hypermobility/instability with Age-related Joint Changes

49
Q

What could surgery be for with osteochondritis dissecans?

A

resurfacing or fixation needed for unstable lesion

50
Q

What is reactive arthritis?

A
  • Aka Reiter’s Syndrome
  • Acute, infection at a site remote from the primary infection
    (Septic arthritis is an infection at the site of primary infection)
51
Q

What are risk factors for reactive arthritis?

A

IV drug users
High sexual activity
Infrequent pelvic examinations
Weaker immune system

52
Q

What does reactive arthritis usually target?

A

targets larger joints in the LE and primarily the knee and ankle

53
Q

What is the etiology of reactive arthritis?

A
  • MOST commonly from a respiratory infection
  • Also, may occur from GI, genitourinary and colon infection
54
Q

What is the pathogenesis of reactive arthritis?

A

bacteria stimulates antibody and protein factor production that creates inflammation and tissue damage leading to an arthritic joint

55
Q

What are clinical manifestations of reactive arthritis?

A
  • Begin 1-4 weeks after a recent infection
  • Infection S&S
  • May progress to incapacitating illness
56
Q

What will we observe with reactive arthritis?

A

Redness
Swelling

57
Q

What will we find with vital signs with reactive arthritis?

A

temperature

58
Q

What will we find in our scan and biomechanical exam with reactive arthritis?

A

Like for Age-related Joint Changes

59
Q

What will we find with palpation with reactive arthritis?

A

TTP and warmth
Swollen and tender lymph node(s)

60
Q

What kind of referral is reactive arthritis?

A

Urgent referral to MD

Clin Med II - FINAL (5 decks)

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