MS FINAL from KW

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248 Terms

1
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<p>what does this x-ray show</p>

what does this x-ray show

osteoarthritis

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<p>what does this x-ray show</p>

what does this x-ray show

something is wrong with the soft tissue

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<p>Which part of the meniscus can be repaired?</p>

Which part of the meniscus can be repaired?

the lateral ridge of both menisci

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What's the trade off with a meniscal repair?

repair=can't weight bear for a few weeks

partial menisectomy=can walk to your car right after

5
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<p>what is wrong</p>

what is wrong

could be muscle strain or a HNP

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difference between cauda equina and HNP

cauda equina comes out medially

HNP comes out laterally

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<p>describe</p>

describe

normal MRI

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<p>what is wrong</p>

what is wrong

there's a compression fracture on the third one down

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<p>what is wrong</p>

what is wrong

vertebral compression fracture

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If the patient says I lost weight without trying and I get night sweats

he has some form of osteosarcoma

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<p>what will happen</p>

what will happen

lateral meniscus will wear out

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<p></p>

medial joint space narrowed

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<p>what is this</p>

what is this

fall on outstretched hand

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<p>what is this</p>

what is this

FOOSH

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<p>describe</p>

describe

no fracture

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<p>describe</p>

describe

FOOSH, distal radial fracture

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<p>what is this</p>

what is this

distal radial fracture

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<p>distal portion of the distal bone pointing towards the dorsum (back) of the hand</p>

distal portion of the distal bone pointing towards the dorsum (back) of the hand

Colles Fractures

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<p>what is this</p>

what is this

colles fracture

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<p>what is this</p>

what is this

open reduction internal fixation (colles fracture)

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MOI of Colles Fracture

FOOSH

<p>FOOSH</p>
22
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<p>what is this</p>

what is this

L5 herniation

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prevalence of OA and RA

OA – 20.7 million

RA - 2.1 million

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osteoarthritis

A degenerative disorder with minimal articular inflammation.

No systemic symptoms.

Pain relieved by rest; morning stiffness brief.

Radiographic findings: narrowed joint space, osteophytes

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OA general information

non-inflammatory disease

characterized by progressive degeneration of joint cartilage with bone margin involvement and osteophyte formation

· Osteoarthritis is a chronic long-term, degenerative disease that causes the breakdown of cartilage in the joints leading to pain and stiffness.

cortical steroids (risk factor for osteoporosis)

Before the age of 45, osteoarthritis predominantly affects men. After 55 the condition is more frequent in women.

Fifty percent of people over 60 years of age are affected in at least one joint. It is estimated that everyone over the age of 75 suffers from osteoarthritis.

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primary osteoarthritis

· an unknown cause but is generally associated with aging. It is sometimes referred to as "wear and tear" arthritis.

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secondary osteoarthritis

the destruction of cartilage from a known cause. Conditions that lead to cartilage loss include repetitive trauma, obesity, crystal deposits, infection, congenital abnormalities, injury or joint surge (obesity, gonorrhea, gout)

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joints most commonly affected include

hips and knees

joints where thumb meets hand (carpometacarpal joint/basal joint), two distal joints to the knuckle

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OA signs and symptoms

Pain

Pain is the most common symptom of osteoarthritis and usually increases with joint use.

Pain can also restrict mobility.

Stiffness

Swelling

Deformity

Painless, irregular bony enlargements

Heberden's nodes

Bouchard's nodes

“Harley-Davidsons raise your Blood Pressure”

Crepitus

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stiffness with OA

Stiffness of the affected joint is often noticed first thing in the morning, and after resting. < 15 minutes

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crepitus

Grating sound or sensation produced by friction between bone and cartilage

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<p>what is this</p>

what is this

eroding cartilage

33
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<p>what is this</p>

what is this

cartilage

34
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<p>what is this</p>

what is this

osteoarthritis

35
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What symptoms can you see on an x-ray?

bone spurs, narrowing space

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Why can't cartilage grow back?

it's avascular

37
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Heberden's nodes

bony growths of DIP

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Bouchard's nodes

bony growths of PIP

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OA risk factors

Obesity

Trauma

Genetics - predilection for cartilage breakdown

Increased age (>40)

Repetitive movements (sports or employment - manual laborers)

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radiograph "LOSS"

a. Loss of joint space

b. Osteophytes - spurs of bone

c. Subarticular sclerosis

Increased density of bone on joint line

d. Subchondral cysts

Small fluid filled holes in bone on the joint line

41
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<p>what is this</p>

what is this

OA on left hip

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OA labs

none

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OA medical treatment

1.Acetaminophen – Tylenol

2. Nonsteroidal anti-inflammatory (NSAIDs)

Motrin

Advil

Celebrex

Intra-articular injections of triamcinolone ((corticosteroid) often

with lidocaine)

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surgical intervention-joint arthroplasty

Total hip and knee replacements provide excellent symptomatic and functional improvement when involvement of that joint severely restricts walking or causes pain at rest, particularly at night.

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What's a risk of arthroplasty?

infection

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micro-fracture surgery

quick fix to help delay an arthroplasty, wet paint on knee, you can't weight bear for a 5 weeks. A lot of people

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OA prognosis

a. No cure

b. Manage pain and minimize disability

c. Maintain quality of life

d. Encourage exercise - strength and joint function

e. Depression associated with chronic pain

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DIP

distal interphalengeal

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rheumatoid arthritis

a chronic, system, autoimmune inflammatory disease

<p>a chronic, system, autoimmune inflammatory disease</p>
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RA essentials

Usually insidious onset with morning stiffness and joint pain.

Symmetric polyarthritis with predilection for small joints of the hands and feet; deformities common with progressive disease.

Rheumatoid factor and antibodies to cyclic citrullinated peptides (anti-CCP) are present in 70-80%.

Extra-articular manifestations: subcutaneous nodules, interstitial lung disease, pleural effusion, pericarditis

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What is the most common inflammatory arthropathy?

rheumatoid arthritis

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Are men or women more likely to get RA?

females (3:1 ratio)

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When is RA onset?

4th or 5th decade

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RA environmental factors

tobacco; known to be a major trigger both for new onset RA and as an exacerbating agent for existing RA

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RA genetic factors

HLA DR beta 1 alleles - genetic trait that increases the incidence of the condition. There is a strong familiar relationship associated with RA. (can be passed on)

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inflammatory response

chronic inflammation of the synovium (synovitis) erodes cartilage, bone, ligaments, and tendons.

Effusion and other manifestations of inflammation are common.

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unbated

without any reduction in intensity or strength (disability becomes pronounced)

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RA symptoms

Patients have flares (OA is constant) RA can get worst sometimes and have asymptomatic days

Usually insidious onset with morning stiffness and joint pain.

Symmetric polyarthritis with predilection for small joints of the hands and feet

Wt loss, fatigue, muscle weakness and vague m/s discomfort that eventually settles in joints

Morning stiffness that lasts about one hour

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What joints are affected by RA?

Although any joint may be affected the most commonly involved joints are:

i. PIP joints of the fingers

ii. MCP joints

iii. Wrists

iv. Knees

v. Ankles

vi. MTPs

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Stages of RA

it's a progressive disease-deformities caused by disruption/erosion of ligaments and tendons

Early RA -> Intermediate RA -> Late RA

<p>it's a progressive disease-deformities caused by disruption/erosion of ligaments and tendons</p><p>Early RA -&gt; Intermediate RA -&gt; Late RA</p>
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Physical exam findings

1. Joint findings (we want to fend off inflammation with medication before deformities occur and we can't help them)

2. Rheumatoid nodules

3. Ocular symptoms

4. Systemic disease (must do a good pulmonary and cardiac exam)

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joint findings

A. Polyarticular joint edema, erythema and pain, often at rest (red, painful, warm to touch)

B Swan-neck and Boutonniere deformities

C Ulnar deviation at MCPs

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Swan neck deformity

hyperextension at PIP and Flexion at DIP

<p>hyperextension at PIP and Flexion at DIP</p>
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Buotonniere Deformity

flexion at PIP and hyperextension at DIP

<p>flexion at PIP and hyperextension at DIP</p>
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ulnar deviation at MCPs

thickening of fingers-sausage fingers, edematous- important to take rings off so they don't have to be cut off

<p>thickening of fingers-sausage fingers, edematous- important to take rings off so they don't have to be cut off</p>
66
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rheumatoid nodules

Twenty percent of patients have subcutaneous rheumatoid nodules, most commonly situated over bony prominences but also observed in the bursae and tendon sheaths

<p>Twenty percent of patients have subcutaneous rheumatoid nodules, most commonly situated over bony prominences but also observed in the bursae and tendon sheaths</p>
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ocular symptoms

Dryness of the eyes, mouth, and other mucous membranes is found especially in advanced disease

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systemic disease

A Interstitial lung disease -decreased ability to gas exchange

B Pericarditis -inflammation of the pericardial sac in which the heart sits

C Disease of the lung pleura

**because the immune system attacks more than joints - thus we must be

concerned with systemic manifestations

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RA classic complaint

I woke up and my ____ was sore and I couldn't move it and I couldn't _____ but now it feels fine (they had a flare but it went away before we saw them)

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RA labs

1 Anti-cyclic citrullinated peptide (anti-CCP)

Anti-CCP antibodies are the most specific blood test for rheumatoid arthritis

Anti-CCP is an autoantibody produced by the patient’s immune system that attacks the body. These attacks can produce inflammatory symptoms most commonly experienced in rheumatoid arthritis.

2 Rheumatoid factor

An antibody that is detectable in the blood of approximately 80% of adults with rheumatoid arthritis.

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RA prognosis

Aggressive RA can shorten life by 10-15 years (cardiac/pulmonary issues)

Decreases quality of life = some depression involved

Early aggressive therapy is warranted by rheumatologist

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RA treatment

“The primary objectives in treating rheumatoid arthritis are reduction of inflammation and pain, preservation of function, and prevention of deformity.”

“Early recognition and diagnosis of RA may allow intervention with appropriate medications with a decrease in the destructive arthropathy that can occur with the disorder.” JAAPA DiBaise and Kohn

If medications do not achieve the target of remission of symptoms or low disease activity, additional medications should be added to the therapeutic regimen.

Immunosuppressive agents increase a patient’s risk of infection including Hepatitis B and Hepatitis C. (should be the first in line for vaccines every year)

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low-dose corticosteroids (prednisone)

produce a prompt anti-inflammatory effect and slow the rate of articular erosion. These should only be used for short term control for patients with acute "flares". (keep in mind they increase risk for osteoporosis)

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disease-modifying antirheumatic drugs (DMARDs)

sulfasalazine, methotrexate, and biological response modifiers

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sulfasalazine

similar to methotrexate in terms of medication category.

This medication is a good choice for women with RA who are interested in becoming pregnant. Sulfasalazine is not teratogenic and will allow her to safely become pregnant.

LFT should be obtained at the onset of medication and then every 3 months thereafter and after increasing the dose.

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methotrexate

a long standing medication used to treat RA

Methotrexate increases adenosine levels. Adenosine

promotes an anti-inflammatory state.

Taken once per week - by mouth or IM injection (thigh)

Adversely impacts body's folic acid levels via GI tract - thus patients often take folic acid supplements along with methotrexate.

Known teratogenic effects make this medication CONTRAINDICATED in pregnancy.

Obtain a pregnancy test prior to starting the medication.

Adverse effect - possible liver damage - pts are often advised to avoid alcohol and monitor LFTs (liver function tests). LFT should be obtained at the onset of medication and then every 3 months thereafter.

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Anencephaly

fetus taken to gestation but born without CNS (lack of folic acid)

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spina bifida

spinal cord grown outside of skin (lack of folic acid)

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What is needed in CNS production?

folic acid

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biological response modifiers

newest class of disease-modifying antirheumatic drugs (DMARDs) used to treat rheumatoid arthritis.

They are genetically engineered to act like natural proteins in the patient’s immune system.

Biologics don’t cure RA, but they can dramatically slow its progression.

Generic Name Trade Name

A Etanercept Enbrel

B Adalimumab Humira

C Infliximab Remicade

*These are injectable medications*

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info about DMARDs

All three of these drugs are tumor necrosis factor blockers. TNF is a protein in the immune system that contributes to inflammation and joint damage. TNF blockers block the action of TNF that leads to damage from abnormal inflammation.

Medications in this class cause the patient to be at increased for serious infections such as tuberculosis, herpes zoster and fungal infections

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What are concerns about a patient on steroids for too long?

impaired immune system and bone density problems

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meniscus

c-shaped wedges of fibrocartilage between tibial plateau and femoral condyle

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What happens to the meniscus over time?

it wears down and joint space narrows

85
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Which meniscus is more likely to tear?

the medial meniscus because it is larger and more tethered down

<p>the medial meniscus because it is larger and more tethered down</p>
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x-ray

shows us things with high levels of calcium

<p>shows us things with high levels of calcium</p>
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magnetic resonance imaging (MRI)

shows us bones and soft tissues (diagnostic modality of choice for soft tissue and thus the knee)

<p>shows us bones and soft tissues (diagnostic modality of choice for soft tissue and thus the knee)</p>
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common age groups affected by meniscal tears

young athletic people or men or women over the age of 55

<p>young athletic people or men or women over the age of 55</p>
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Why are older people affected by meniscus tears?

the meniscus gets thinner as we get older so it's more likely to tear

<p>the meniscus gets thinner as we get older so it's more likely to tear</p>
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MOI

mechanism of injury

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meniscal tears MOI

a rotational force

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Are all meniscal tears the same?

no

<p>no</p>
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symptoms of meniscal tear

Locking (difficulty bending)/popping

Will feel weak but if asked to stand on it will not fall to the ground (ACL tears you will fall to the ground)

Catching

Painful clicking

“Giving way”

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signs of meniscal tear

Edema/Hemarthrosis: develops gradually slower than ACL

(will happen much later than an ACL tear-those usually happen within minutes to first hour) takes much longer than an hour

decreased range of motion

McMurray Test, Thessaly Test

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hemarthrosis

blood within a joint

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decreased ROM for meniscus

evaluate ability to fully extend - a meniscus injury can block full extension

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non-surgical treatment for torn meniscus

RICE - - with no mechanical symptoms and in the case of a degenerative tear

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RICE

rest (crutches, relax), ice (15-20 minutes), compression (compression sleeve), elevation (laying supine and raise injury above level of heart)

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surgical treatment for meniscal tear

arthroscopic debridement or repair

<p>arthroscopic debridement or repair</p>
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How many ports enter the knee in arthroscopic surgery?

1. camera

2. irrigating instrument (lets in sterile saline)

3. trimming instrument

<p>1. camera</p><p>2. irrigating instrument (lets in sterile saline)</p><p>3. trimming instrument</p>