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Semester 3 > orthopedic pathology (joint pathologies) > Flashcards

orthopedic pathology (joint pathologies) Flashcards

1
Q

joint pathologies

A

..

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2
Q

types

A

degenerative
(Osteoarthritis)

inflammatory
(Reumatoid arthritis, Ankylosing spondylitis, Psoriatic arthritis)

metabolic
(Gout, pseudogout)

infectious
(Septic arthritis)

neurogenic
(Charcot’s arthropathy)

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3
Q

OA, aka

A

DJD

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4
Q

abut OA

A

Chronic, degenerative condition that affects joints, specifically articular cartilage and subchondral bone

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5
Q

what structure particularly affet

A

articular cartilage
subchondral bone

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6
Q

prealance increaes with

A

age

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7
Q

MOST COMMON JOINT DISORDER IS???

A

OA

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8
Q

primary vs seconary OA

A

Primary OA – idiopathic

Secondary OA – to joint trauma, infection, hemarthrosis, osteonecrosis, etc.

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9
Q

primary OA

A

MOST COMMON

via regualr wear/tear

caused by the breakdown of cartilage

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10
Q

secondary OA

A

caused by another disease, infection, injury, or deformity. Osteoarthritis starts with the breakdown of cartilage in the joint.

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11
Q

seconary via

A

joint trauma, infection, hemarthrosis, osteonecrosis, etc.

also eg
RA cause OA (?)

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12
Q

risk factors OA

A

joint immobilization

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13
Q

jint immobilziatson oa

A

Conclusions. Joint immobilization caused multiple OA-like lesions in both mice and humans. Joint immobilization induced progressive sensory innervation, synovitis, osteophyte formation, and cartilage loss in mice, which can be partially ameliorated by remobilization.

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14
Q

other isk fators

A

Altered biomechanics – developmental deformities; Genu valgum/varus

Immobilization

Trauma

Pathology

Genetics – familial forms of some hand OA

Gender – mc in women over age 50

Lifestyle- obesity (high correlation w/ knee OA and even hand OA)

Low vitamin D and Vitamin C intake are associated with increased risk of knee OA progression

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15
Q

which vitamin definicency, OA

A

Low vitamin D and Vitamin C intake

knee OA progression

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16
Q

OA define

A

can be defined as a gradual loss of articular cartilage, combined with thickening of the subchondral bone, bony outgrowths (osteophytes) at joint margins, and mild, chronic nonspecific synovial inflammation.

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17
Q

other features of oa

A

osteophytes (exostosis)

nonsepcific synovial infalmation

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18
Q

OA part of

A

aging

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19
Q

can you distinguish bw oa and aging

A

3 states identified

normal cartiage –> aginng cartilage –> OA cartilage

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20
Q

pathogeneiss OA

A

Phase 1: Edema and Microcracks

Edema of the extracellular matrix

Cartilage loses its smooth aspect and microcracks begin to appear

Cartilage softens and thins
Loss of joint space

There is a focal loss of chondrocytes

Unable to repair as normal

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21
Q

phase 2

A

Phase 2: Fissuring and Pitting

Microcracks deepen perpendicularly in the direction of tangential forces and along collagen fibers

Vertical clefts form in the cartilage above the subchondral bone

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22
Q

phase 3

A

Phase 3: Erosion

Fissures cause fragments of cartilage to detach off; causing:
Osteocartilaginous loose bodies

—> Synovial inflammation (often more focal than inflammation occurring due to rheumatoid synovitis)

—> Inflammation caused synovial hypertrophy and capsular thickening

Uncovering subchondral bone:
—> Sclerosing of subchondral bone

—> Subchondral cysts

—> Osteophyte formation

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23
Q

Dx oA

A

History
Physical exam
Lab tests
X-ray

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24
Q

Sx

A

Pain is the cardinal symptom of OA and is the major determinant of disability and functional impairment

Pain is not always present in patients with radiographic findings

Degree of radiographic findings does not always correlate with clinical symptoms

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25
Q

IMPORTANT NOTE: IS BAD OA ALWAYS WITH PAIN

A

no, very bad OA might not have proporitonal pain

and very mild OA might have a lot of pain

RADIOGRAPHIC FINDINGS NOT PROPORTIONAL WITH PAIN

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26
Q

mechanisms of pain?

A

multifactoral and may include:

Periostitis (bone remodeling)

Subchondral microfractures

Synovial inflammation

Periarticular muscle spasm

Bone ischemia

Elevated interosseus pressure

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27
Q

SSx OA

A

Monoarticular or polyarticular

Joint pain (usually relieved w/ rest)

Tenderness

Crepitus

Occasional effusion

Variable degrees of local inflammation

Bony enlargement

Stiffness (morning stiffness- less than 30min)

Decreased ROM

Deformities; misalignment

Muscle spasm/contractures

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28
Q

how long stiffness last OA

A

usually less than 30 mins

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29
Q

ROM OA

A

decrease

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30
Q

muscle spasms/conttractures OA

A

yes (bracing/protective spasms to avoid pain)

contractures due to prolonged limited ROM?

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31
Q

crepitus?

A

a grating sound or sensation produced by friction between bone and cartilage or the fractured parts of a bone.

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32
Q

common features/locaitons

hand

A

Heberden’s nodes at distal IP joint accompanied by lateral joint deviation

Bouchard’s nodes found at proximal IP joint

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33
Q

knee

A

Pain worsens with stair climbing, standing

Highly associated w/ obesity

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34
Q

spine

A

Vertebrae of L4, L5, C4-C7, upper T-spine

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35
Q

hip

A

Internal rotation and extension are reduced

note CPR:
mr/abd, f/e, er

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36
Q

treatment oa

A

Analgesics
Topical creams/gels
NSAIDs
Corticosteroids

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37
Q

other tx

A

Exercis:
Strengthening, low impact ROM exercise

Avoid stress on joints

Control weight

Warm-up/cool down

Ice

Pacing

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38
Q

note the dilemma

A

exercises that are good for osteoporosis cna be bad for OA

activiites that are good for OA, while not bad for osteoporosis, will not prevent it as well

either OA develops quicker, or osteoporosis

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39
Q

other tx OA, hydro surgery, complementary therapy (Vs allotherapy)

A

Hydrotherapy
Heat/cold (chronic)

Surgery
Clean up (arthroscopy) or replace joint

Complementary therapy
Acupuncture
Massage
Mobilization/manipulation
PT
chiro (?)

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40
Q

RA

A

A systemic inflammatory disease that predominantly manifests in the synovial membrane of diarthrodial joints

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41
Q

important feature of RA

A

hyperplasia of synovial fibroblasts

structural damage of cartilage, bone, and ligaments

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42
Q

where else?

extra articular manifestation

A

can effect a variety of organs and is a significant factor in morbidity and mortality of people w/ RA

Esp kidneys

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43
Q

etiolgoy

A

genetic + viral (?)

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44
Q

gender RA

A

Women > men (3:1)

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45
Q

age RA

A

ny age, prevalence incr. with age (25-50)

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46
Q

RA onset, remission

A

Onset gradual

Symptom free for months or years

Exacerbations and remissions

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47
Q

RA prognosis

A

Prognosis uncertain

Death can occur from extra-articular disease

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48
Q

RA and immune response

A

aberrant immune response in a genetically predisposed host that leads to chronic progressive synovial inflammation and destruction of joint archeticture

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49
Q

synovium and RA

A

Primary inflammatory lesion involves the synovium

Edema, fibrin exudation and hyperplasia of synovium

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50
Q

what type of exudate RA , where?

A

fibrin exudation and hyperplasia of synovium

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51
Q

other common feature/sx

A

Tenosynovitis is present in a majority of patients

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52
Q

extraarticualr menif

A

Extra-articular manifestations are common but individuals differ in the pattern of tissues involved

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53
Q

Ssx RA

A

Pain
Warm, red, swollen, tender joints

tiffness
Morning stiffness usually lasting more than 2 hours

Structural damage
Cartilage loss and erosion of periarticular bone (evident on xray)

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54
Q

how long morning stiffness

A

more than2 hours

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55
Q

where often begin RA

A

Often begins in hands and wrists

Usually symmetrical and uniform

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56
Q

most common site

A

PIP, MCP, wrists, knees, MTP, subtalar, C1, C2

(TV LIGAMENT OF C1-C2 articulation)

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57
Q

Han ddefomirtities

A

Swan neck – PIP hyperextended, DIP flexed

Boutonniere (buttonhole) – PIP flexed, DIP hyperextended

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58
Q

other ssx

A

tendon/muscle spasm (REFLEX MUSCLE GUARDING?)

Contracture (scar tissue, inflammation immune damage)

Subluxations and deformities may develop
Knee valgus

Baker’s cyst
d/t inflamed synovium

Neck pain
Unstable C1-C2 (important to rule out prior to mobilization/adjustments of upper cervical complex)

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59
Q

IMPORTANT CYST ASSOCIATED WITH RA

A

Baker’s cyst
d/t inflamed synovium

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60
Q

IMPORTANT LIGAMENT ASSOCIATED WITH RA NECK PAIN

A

TRANSVERSE LIGAMENT OF ATLAS

Unstable C1-C2 (important to rule out prior to mobilization/adjustments of upper cervical complex)

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61
Q

extra articular SSx

A

Rheumatic nodules

Develop in 50% of individuals

Form subcutaneously, in bursae and along tendon sheaths

Systemic symptoms include aching, stiffness, weight loss, fatigue

Ocular manifestaions
Dry eyes

Pericarditis
Pleurisy and laryngeal pain

Renal complications
Rare

Weight loss
Anemia

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62
Q

inflammation of SEROUS membranes

A

PERICARIDUM

pleura

Pleuritis (Pleurisy)

pericarditis

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63
Q

rheumatic nodules, devleop in what percentage of patients

A

Rheumatic nodules

Develop in 50% of individuals

Form subcutaneously, in bursae and along tendon sheaths

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64
Q

RA why dry eyes

A

Inflammation from RA causes abnormalities in the tear glands (lacrimal), significantly reducing fluid secretion

The symptoms associated with dry eyes are more common in the later part of the day, when tears from the tear gland (systemic) have dried up and evaporated.

65
Q

RA why anemia

A

RA can be associated with different types of anemia, including anemia of chronic inflammation and iron deficiency anemia.

When you have an RA flare-up, the immune response causes inflammation in the joints and other tissues.

Chronic inflammation can lower the production of red blood cells in your bone marrow.

66
Q

RA Dx

A

family history

Lab tests:
rheumatoid factor – present in 85% of people w/ RA

ESR & C-reactive protein

X-ray, imaging

67
Q

C reactive protein test

A

C-reactive protein (CRP) is a protein made by the liver. The level of CRP increases when there’s inflammation in the body

68
Q

ESR test (erythrocyte sedimentation rate)

A

What Is an ESR Test? An ESR test measures how far red blood cells settle to the bottle of a test tube in 1 hour.

Inflammation or infection can lead to extra proteins in the blood, which can make the red blood cells settle farther in a test tube. When this happens, the ESR is higher.

69
Q

rheumatoid factor test

A

This test measures rheumatoid factors in a sample of your blood. High levels of rheumatoid factors may be a sign of rheumatoid arthritis

70
Q

Tx RA

A

Corticosteroids to decrease inflammation and pain

Immunosuppressive drugs

NSAIDs

Surgery

Physiotherapy

71
Q

RA prognosis

A

Difficult to establish d/t chronic nature of the disease, its variability and the difficulty in identifying milder forms

Spontaneous remission is possible
Approx 10% of cases

90% of joints affected are usually involved within the first few years of the disease

Patients with severe forms have a mortality rate approx 10 -15 years earlier than expected and d/t infections, pulmonary, renal, and gastrointestinal bleeding.

72
Q

remission in what percentage

A

Spontaneous remission is possible
Approx 10% of cases

73
Q

ankylosing spondylitis (AS)

etymology

A

ankylos meaning crooked, curved or rounded, spondylos meaning vertebra, and -itis meaning inflammation

74
Q

AS affects

A

systemic disorder characterized by inflammation of the axial skeleton (SI joints, facets, IVDs) and large peripheral joints.

75
Q

Seronegative spondyloarthropathy

A

MEDICINE
adjective: seronegative
giving a negative result in a test of blood serum, e.g. for the presence of a virus.

Spondyloarthropathies are a family of long-term (chronic) diseases of joints. These diseases occur in children (juvenile spondyloarthropathies) and adults. They include ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and joint problems linked to inflammatory bowel disease (enteropathic arthritis).

76
Q

Seronegative spondyloarthropathies

A

Seronegative spondyloarthropathies (SpA) are a family of rheumatologic disorders that classically include[1]: Ankylosing spondylitis (AS) Psoriatic arthritis (PsA) Inflammatory bowel disease (IBD) associated arthritis. Reactive arthritis (formerly Reiter syndrome; ReA)

77
Q

ankylosis spondylitis

A

Ankylosis - immobility and fixation of a joint

Spondylitis - inflammation of the vertebrae

78
Q

AS gender

A

Men > women (3:1)

Onset insidious

79
Q

AS age

A

Typically occurs between ages 20 – 40

Average age is 26

80
Q

remissions or no

A

Development variable

Exacerbations and remissions

Can lead to deformities

81
Q

ettiology/cause

A

Idiopathic

genetic/ environmental

“Has genetic component (20% increased risk w/ 1st degree relative), but thought to be influenced by environmental factors”

82
Q

HLA-B27 test

Human Leukocyte Antigen; subtype B27

A

The HLA-B27 test is primarily ordered to help strengthen or confirm a suspected diagnosis of ankylosing spondylitis (AS), reactive arthritis, juvenile rheumatoid arthritis (JRA), or sometimes anterior uveitis.

“Human leukocyte antigen B27 is a class I surface molecule encoded by the B locus in the major histocompatibility complex on chromosome 6 and presents antigenic peptides to T cells. “

83
Q

ENTHESES ???????????????????????

A

Entheses are boney insertion sites of tendons and ligaments.

Enthesopathies are defined as the pathologies that affect the entheses.

ENTHESIS

“Enthesis” is rooted in the Ancient Greek word, “ἔνθεσις” or “énthesis,” meaning “putting in,” or “insertion.”

84
Q

AS pathogneesis

A

Inflammation at the entheses is the central feature of AS (enthesitis)

(Entheses is the site where tendons and ligaments attach to bone.)

85
Q

then what

A

Inflammation of ligaments results in fibrosis, bony erosions and eventually causes reactive bone growth and spurring

86
Q

WHAT CAN HAPPEN EVENTUALLY

A

Eventual fusion of joint can occur

87
Q

where usualyl begin ******

A

Usually begins in the lumbar spine and SI joints (sacroiliitis) and proceeds up the spine (over years)

88
Q

AS and back pain

A

Insidious onset

Persistent for more than 3 months

Worse at night and w/ inactivity

Improved by activity

89
Q

UNIQUE about AS (AS and ACTIVITY LEVELS)

A

Worse at night and w/ inactivity

Improved by activity

90
Q

L spine stiffness in morning and time to improve

A

L-spine stiffness:

Typically AM

Takes more than 2 hours to get better

91
Q

pain in posteiror thigh?

A

Pain in buttocks, low back, post. thigh

referral?)

92
Q

what are some changes to spine posture?

A

thoracic hyperkyphosis
lumbar hypolordosis

Lumbar lordosis lost
Thoracic curve increases
Flexion contracture (hips)

93
Q

AS and breathing problems

A

note fusion of vertebrae and surround joints/structures of costovertebral joints

Chest is fixed/flattened
Chest expansion limited

“Trouble breathing as the upper body curves forward and the chest wall stiffens. Severe ankylosing spondylitis can also cause scarring of the lungs (pulmonary fibrosis) and an increased risk of lung infection.”

94
Q

decreased ROM of spine and pain

A

Pain diminishes over the years as fusion occurs

Muscle wasting

Fatigue

95
Q

complications AS

A

Osteoporosis, fractures, stenosis, C1-C2 subluxation

96
Q

SPINAL STENOSIS

A

Spinal stenosis happens when the space inside the backbone is too small. This can put pressure on the spinal cord and nerves that travel through the spine. Spinal stenosis occurs most often in the lower back and the neck.

“In severe cases, spinal stenosis may cause partial or complete leg paralysis that requires emergency medical treatment.”

97
Q

AS c1-c2 subluxation

A

In ankylosing spondylitis, cervical spine can be involved and may progress to C1-C2 subluxation, also known as atlantoaxial subluxation, with a prevalence ranging from 13.8 to 21% in adults [5–8].

98
Q

what percentage systemic manifestation

A

30% 1/3

99
Q

which parts affected?

A

Uveitis, iritis, conjunctivitis
Inflammation of eyes
Pain, blurred vision, blindness

Large and small bowel disease

Cardiovascular involvement

100
Q

is AS autoimmune?

A

Ankylosing spondylitis is an autoimmune disease.

101
Q

Dx AS

A

History

Phiscal exam

Lab :
HLA B27 test

X-rays
Bamboo spine – vertebrae take on a fused appearance

102
Q

Tx AS

A

Meds (anti-inflammatories)

Massage/Chiro/Physio

Sleep on hard mattress or cold floor (during inflammation)

Exercise, stretching

Breathing exercises

Surgery (severe cases)

103
Q

AS breathing

A

Breathing exercises

104
Q

AS where to sleep during flareup

A

Sleep on hard mattress or cold floor (during inflammation)

105
Q

Psoriatic arthritis

A

Is an arthritis often associated with psoriasis of the skin

106
Q

psoriasis

A

a skin disease marked by red, itchy, scaly patches.

107
Q

psoriasis and arthritis

A

1 in 20 will develop arthritis with the skin condition

108
Q

cause

A

idiopathic

109
Q

psoriatic arthritis affects

A

Primarily affects distal joints of fingers and toes

When spine is affected (L/S and sacrum)

Stiffness, burning, pain

110
Q

psoriatic arthritis Dx, Tx

A

same in men and women

Dx
Physical exam, joint swelling, skin sores

Tx
NSAIDS

Antirheumatic drugs
—> E.g. Methotrexate

Steroids

Surgery

RMT, PT, Hydro

111
Q

polyarthritis define

A

the medical term for having arthritis that affects five or more of your joints at the same time

112
Q

Gout (METABOLIC ARTHRITIS)

A

group of disorders in which crystals of monosodium urate (uric acid) are deposited in the tissues, accompanied by attacks of acute arthritis

113
Q

where does uric acid go

A

Marked by an elevated level of serum uric acid and the deposition of urate crystals in the joints, soft tissue AND KIDNEYS

114
Q

normal presence of uric acid

A

Uric acid is normally formed with the break down of purines (Adenine, Guanine)

Uric acids dissolves in the blood, passes through the kidneys and is then excreted

115
Q

abnormal presence of uric acid

A

With too much production or with poor kidney function uric acid may precipitate out and accumulate in body tissues

Crystals frequently collect on articular cartilage

These trigger an inflammatory response resulting in local tissue necrosis and proliferation of fibrous tissue (scar tissue?)

116
Q

tophi (tophus)

A

Tophi are ordered aggregates of monosodium urate (MSU) crystals that develop in long-lasting, neglected gout.

Most of them are subcutaneous and involve the feet, hands, knees, and elbows.

They are a feature of advanced gout and indicate a large crystal load.

117
Q

1) primary hyperuricemia

A

Inherited disorder of uric acid metabolism

118
Q

2) Secondary hyperuricemia

A

Occurs as a result of some other metabolic problem

Increased DNA turnover via Leukemia, lymphoma, chemotherapy

119
Q

3) Idiopathic hyperuricemia

A

..

120
Q

cause gout (metabolic arthritis)

A

Can be the result of urate overproduction or decreased urinary excretion of uric acid

121
Q

note intracellular accumulation (?) uric acid underexretion, oversecretion, underutilization (?)
and gout (?)

A

..

122
Q

risk factors

A

Diet rich in purines (adenine, guanine)

Nitrogen containing compounds found in foods

Purine-containing foods: red meats, organ meats, shellfish, sweet breads, dairy, beer

123
Q

gender distribution, gout (Metabolic arthritis)

A

Male > female – 9:1

Usually 40-50 years

124
Q

other risk factors, gout

A

Obesity

Excessive weight gain, especially with puberty

Moderate-heavy alcohol intake

Hypertension

Abnormal kidney function

Certain medications

125
Q

more risk factors

A

Certain diseases - lymphoma, leukemia, hemoglobin disorders

—> Increased nuclear-protein turnover

Decreased thyroid function

Dehydration

Excessive dining

126
Q

gout and kidney stones

A

Studies have shown that patients with gout are 60 percent more likely to develop kidney stones.

Kidney stones, also known as renal lithiasis, are similar to gout in that they are both related to a high concentration of uric acid in the blood.

127
Q

most common where?

A

Most common - first MTP joint

Can also affect fingers, wrists, elbows, ankles, knees

128
Q

onset of pain, and inflammation

A

Rapid onset pain, swelling, heat, redness, tenderness, +/- fever

129
Q

tophi…

A

Nodular masses of uric acid depositing in soft tissues of body - tophi

130
Q

is gout unilateral or bilateral

A

Tends to be unilateral

can be bilateral (..)

131
Q

gout (metabolic arthritis) diagnosis

A

differential diagnosis (DDx)
—> RULE OUT OTHER POSSIBILITIES

E.g.
Septic (Infectious) Arthritis,
RA,
neoplasm (vs tophi)

132
Q

important diagnostic tools

A

Monosodium urate crystals (tophi) are found within synovial fluid, connective tissue or articular cartilage

Serum uric acid levels are elevated

133
Q

Gout treatment

A

To end acute attacks and prevent recurrent attacks (NSAIDS, Colchicine)

correct the hyperuricemia

134
Q

Colchicine

A

a yellow compound present in the corms of colchicums, used to relieve pain in cases of gout.

135
Q

Gout, Tx

A

Adequate fluid intake

Weight reduction

Dietary changes

Decrease alcohol (increases purine catabolism)

NSAIDS, corticosteroid injections, colchicine

Uric acid inhibitors (allopurinal)

136
Q

infectious arthritis (SEPTIC ARTHRITIS)

A

Joint inflammation as a result of infection

Can be due to bacteria, fungus, virus

137
Q

bacterial pathogens vs septic arthritis

A

Staphylococcus aureus - the most common cause in adults
(Staph Infection)

Haemophilus influenzae - the most common cause in children

Neisseria gonorrhoea - in sexually active young adults

138
Q

other bacterial pathogens vs septic arthritis

A

Escherichia coli - in the elderly, IV drug users and the seriously ill
(E. coli)

M. tuberculosis - Cause septic spinal arthritis (Pott’s Disease)

Streptococcus

Gonococcus

139
Q

how does infection get into joint for spetic arthritis

A

septicemia (blood poisoning)

blood poisoning, especially that caused by bacteria or their toxins.

the presence of microorganisms or their toxins in the blood, causing disease; septicemia.

140
Q

how else does infection get into joints

A

Direct infection – needle users

Iatrogenic – medical treatment

Catheters

Trauma

Immunocompromised patients

141
Q

Direct infection – needle users

Iatrogenic – medical treatment

Catheters

A

during medical treatment

insufficient protocols

142
Q

pathogenesis, septic arthritis

A

Bacteria adheres to synovium:

Leads to scar tissue and synovium proliferation

Hydrolysis of proteoglycans and collagen (breaks down articular cartilage)

Cartilage and bone destruction occur:

Takes a very short time for joint death and direct pressure necrosis

143
Q

infective arthritis clinical manifestations

A

Acute onset of joint pain, swelling, tenderness, loss of motion

Males and females (equal?)

Fever, chills

Pus

Skin lesions

Polyarthralgia

Joints primarily affected:
Shoulders, knee, hips (proximal joints)

144
Q

Infective arthritis Dx

A

PE - pain, swelling, redness in joint

History - STI’s, IV drug use, IC state, surgery, trauma

Blood test - increased WBC count, high RBC sedimentation rate
—> ESR TEST

Fever

Aspirate and culture synovial fluid

X-ray

145
Q

Aspirate and culture synovial fluid (Synovial Fluid Analysis)

A

Gram stain and bacterial culture: synovial fluid aspirate is analyzed for gram stain and both aerobic and anaerobic culture to determine the presence of infection; the presence of any organism indicates abnormal findings.

146
Q

Infective arthritis Tx

A

Medical emergency

Antibiotics via IV

Drain infected joint to decrease pain

Rest

147
Q

infective arthritis prognosis

A

Acute nongonococcal bacterial arthritis can destroy articular cartilage, permanently damaging the joint within hours or days

148
Q

”

A

Although it’s rare, septic arthritis is a serious condition. It can cause permanent damage to your affected joint and other complications.

It can also cause death if it’s not treated. Be sure to see your healthcare provider or go to the nearest hospital immediately if you experience symptoms.

149
Q

antibiotics

A

Septic arthritis often needs treatment right away with antibiotics. This can improve symptoms within 48 hours. Some infections caused by fungi need treatment with antifungal medicine. Viral infections are not treated with medicine.

Antibiotics often stop the infection in a few days, but in some cases, they must be given over several months. Infectious arthritis caused by a virus usually goes away on its own with no specific treatment and fungal infections are treated with antifungal medication. Joint Drainage.

150
Q

Charcot disease

A

Aka Charcot’s arthropathy, neuropathic arthropathy

Progressive degeneration of the stress-bearing portion of a joint

Most commonly associated with diabetic neuropathy

Most commonly occurs in the foot

151
Q

charcot

A

Involves bone destruction and absorption leading to deformity, dislocation, ulcerations, bone fragments and a unstable joint

Cause
Any condition that decreases peripheral sensation, proprioception and fine motor control

152
Q

most common cause

A

DM neuropathy m/c

153
Q

diabetic neuropathy

A

.

154
Q

first theory of underyling mechanism

A

Neurotrauma: Loss of peripheral sensation and proprioception leads to repetitive microtrauma to the joint in question; this damage goes unnoticed by the neuropathic patient, and the resultant inflammatory resorption of traumatized bone renders that region weak and susceptible to further trauma. Indeed, it is a vicious cycle. In addition, poor fine motor control generates unnatural pressure on certain joints, leading to additional microtrauma.

155
Q

second theory of underyling mechanism

A

Neurovascular: Neuropathic patients have dysregulated autonomic nervous system reflexes, and de-sensitized joints receive significantly greater blood flow. The resulting hyperemia leads to increased osteoclastic resorption of bone, and this, in concert with mechanical stress, leads to bony destruction.

156
Q

both mechanisms?

A

In reality, both of these mechanisms probably play a role in the development of a Charcot joint.

157
Q

charctor SSx

A

Swelling, warmth, redness,

subluxation/dislocation, deformity, fractures

Complications:
joint infections, hemarthrosis, septicemia

158
Q

tx charcot

A

.

159
Q
A

Semester 3 (32 decks)

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