ICL 8.8: Osteoarthritis & Cristal Induced Arthritis

Question 1

what is osteoarthritis?

Answer 1

the most common form of arthritis

it’s a degenerative joint disease, occurring primarily in older individuals, characterized by erosion of the articular cartilage, hypertrophy of bone at the margins (i.e., osteophytes), subchondral sclerosis, and a range of biochemical and morphologic alterations of the synovial membrane and joint capsule

it is strongly associated with aging and typically affects the knee, hip, spine, great toe, and hands

Question 2

what parts of the body are more likely to be effected by osteoarthritis in african americans?

Answer 2

blacks more likely to have knee osteoarthritis but less likely to have hand osteoarthritis compared with whites

Question 3

what part of the body is most often effected by osteoarthritis?

Answer 3

1. knee
2. hip
3. hand

Question 4

how does osteoarthritis increase mortality?

Answer 4

mortality is increased in individuals with osteoarthritis compared with the general population

higher mortality was associated with increasing age, male sex, walking disability, and self-reported comorbidities (diabetes, cancer, cardiovascular disease)

increased mortality risk appears to be primarily due to cardiovascular and gastrointestinal causes.

Question 5

what components of the joints are effected by osteoarthritis?

Answer 5

all the components of the joint

1. Bone
2. Cartilage
3. Synovium
4. Capsule
5. Meniscus

Question 6

what factors effect OA?

Answer 6

1. Age
2. Joint location
3. Obesity
4. Genetic predisposition
5. Joint malalignment
6. Trauma
7. Gender

Question 7

what is the genetic effect on OA?

Answer 7

twin pair and family risk studies have indicated that the heritable component may be on the order of 50% to 65%

family, twin, and population studies have indicated differences among genetic influences that determine the site of OA (hip, spinal, knee, hand)

genetic studies have identified multiple gene variations associated with an increased risk of OA [ Collegen 2,4,5,6, Vit D , IGF-1 ETC]

Question 8

how do biomechanics factors effect OA?

Answer 8

mechanical loading that is either below or in excess of the physiologic range causes cartilage degeneration

for this reason, abnormalities of mechanical loading are central to the development of OA

OA arises when there is an imbalance between the mechanical forces within a joint and the ability of the cartilage to withstand these forces

this arises in two situations: either normal articular cartilage is exposed to abnormal mechanical loads or the articular cartilage is fundamentally defective with biomaterial properties that are insufficient to withstand normal load bearing

Question 9

what are the different types of loading modes?

Answer 9

1. tensile loading = pulling apart
2. compressive loading = squishing
3. shear loading = ripping in half

Question 10

what are the two types of lubrication in the joints of the body?

Answer 10

1. boundary lubrication

2. fluid film lubrication

Question 11

what is boundary lubrication?

Answer 11

boundary lubrication is achieved by a macromolecular monolayer attached to each articular surface

looks like a fluid pocket

these layers carry loads and are effective in reducing friction

Question 12

what is a diarthrodial joint?

Answer 12

a joint in which the opposing bony surfaces are covered with a layer of hyaline cartilage or fibrocartilage within a joint cavity that contains synovial fluid, lined with synovial membrane and reinforced by a fibrous capsule and ligaments; and there is some degree of free movement possible

Question 13

what kind of lubrication do diarthrodial joints have?

Answer 13

a mixed mode of lubrication occurs

the joint surface loads being sustained by fluid film pressures in areas of noncontact and by boundary lubrication in areas of contact

Question 14

what are the early changes you see in cartilage in an OA patient?

Answer 14

1. swelling of articular cartilage
2. loosening of collagen framework
3. chondrocytes increase proteoglycan synthesis but also release more degradative enzymes
4. increased cartilage water content

Question 15

what are the late changes you see in cartilage in an OA patient?

Answer 15

1. degradative enzymes break down proteoglycan faster than it can be produced by chondrocytes, resulting in diminished proteoglycan content in cartilage
2. articular cartilage thins and softens (joint space narrowing on radiographs will be seen eventually)
3. fissuring and cracking of cartilage. Repair is attempted but inadequate
4. underlying bone is exposed, allowing synovial fluid to be forced by the pressure of weight into the bone

Question 16

what happens when the extracellular matrix of cartilage breaksdown in OA?

Answer 16

1. loss of compressive stiffness and elasticity, resulting in greater mechanical stress on chondrocytes
2. an increase in hydraulic permeability, resulting in loss of interstitial fluid during compression and increased diffusion of solutes through the matrix (including the movement of degradative enzymes and their inhibitors)

Question 17

what changes in bone are seen during OA?

Answer 17

osteophytes

these are bony proliferations at the joint margins and in the floor of cartilage lesions—are in part responsible for the pain and restriction of joint movement in OA

osteophytes may result from penetration of blood vessels into the basal layers of degenerating cartilage or as a result of abnormal healing of stress fractures in the subchondral trabecular near the joint margins

Question 18

what is subchondral bone sclerosis?

Answer 18

increased remodeling and hardening of subchondral bone is evident early in osteoarthritis and can sometimes be detected before loss of cartilage thickness is evident radiologically

Question 19

what are bone marrow lesions a sign of?

Answer 19

OA

studies suggest that they contribute to the pain felt by OA patients

Question 20

how do you diagnose OA?

Answer 20

the diagnosis of OA is a clinical one

the purpose of additional diagnostic testing in OA is primarily to exclude potentially treatable underlying conditions such as metabolic or inflammatory arthropathies

Question 21

what is the clinical presentation of OA?

Answer 21

1. pain in involved joints
2. pain is worse with activity but better with rest
3. morning stiffness; less than 30 minutes
4. stiffness after periods of immobility = gelling
5. bony joint enlargement
6. joint instability
7. limitation of joint mobility
8. periarticular muscle atrophy
9. crepitus

Question 22

how do you treat OA?

Answer 22

no treatment available for structural damage

only symptomatic treatment available

Question 23

how can you supportively treat knee OA?

Answer 23

1. weight loss
2. exercises
3. adjustment in daily activity
4. orthotics and brace
5. cane walking aid
6. psychosocial Intervention

Question 24

how can you supportively treat hip OA?

Answer 24

1. Weight loss
2. Exercises
3. Adjustment in daily activity
4. Physical therapy
5. Psychosocial
6. Intervention

Question 25

how can you surgically manage OA?

Answer 25

indications for surgery include pain that is refractory to the previously discussed interventions and significant impairment of the patient’s daily life joint replacement surgery (joint arthroplasty) is effective in providing pain relief and restoring function in many patients with OA hip and knee joint replacements are most common

Question 26

how is obesity a risk factor for OA?

Answer 26

it's a strong risk factor especially for your knees which causes mechanical loading and Inflammation activated adipose tissue increases the synthesis of proinflammatory cytokines [ leptin, adiponectin, resistin, interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF), IL-10 are decreased]

Question 27

what lab features are seen in OA?

Answer 27

1. erythrocyte sedimentation rate (ESR) typically within normal limits 2. rheumatoid factor (RF) is negative 3. antinuclear antibodies (ANAs) are not present 4. synovial fluid is normal; normal viscosity with good string sign, color is clear, no crystals, negative cultures

Question 28

what are the common sites for primary OA?

Answer 28

1. neck 2. lumbar spine 3. hips 4. knee 5. DIP and PIP and big toe

Question 29

what is crystal induced arthropathy?

Answer 29

a group of disorder characterised by deposition of crystal inside the joint or soft tissue leading to articular or periarticular tissue inflammation and injury

Question 30

what are the different crystalline arthritis diseases?

Answer 30

1. gout = uric acid 2. CPPD = calcium pyrophosphate there's others too but these are the main ones

Question 31

what is the clinical presentation of crystalline arthritis diseases?

Answer 31

rapid development of severe joint pain, swelling and tenderness that reaches its maximum within 6–24 h, especially with overlying erythema this is highly suggestive of acute crystal inflammation though not specific for crystal arthritis most common presentation is monoarticular but it can be oligoarticular or polyarticular

Question 32

how do you diagnose crystalline arthritis diseases?

Answer 32

1. Clinical symptoms and sign 2. Radiology-X ray, Ultrasound, DECT 3. Confirmation- Aspiration and polarized microscopy 4. 2015 ACR Gout Classification Criteria calculator

Question 33

what other diseases cause monoarticular joint inflammation?

Answer 33

1. bacterial arthritis 2. gonococcal arthritis 3. crystal arthritis 4. tuberculous arthritis aspiration of the joint is a MUST

Question 34

what is the next step if a patient presents with polyarticular inflammatory arthritis?

Answer 34

you do not have to do an aspiration of the joint! it's rarely going to be septic arthritis

Question 35

what is gout?

Answer 35

uric acid build up dietary purines (meat) --> purine nucleotides and bases --> uric acid pool uric acid is eliminated 70% via renal excretion and 30% via gut elimination but if there's an overproduction of uric acid or under secretion then monosodium crystals can form and deposit in the joints

Question 36

what are the stages of gout?

Answer 36

asymptomatic hyperuricemia --> acute intermittent gout --> advanced gout persistent low-grade inflammation with relatively short periods of acute severe inflammation 10 years or longer before progression to the chronically symptomatic

Question 37

what are the comorbities of gout?

Answer 37

for more than a century, gout has been associated with hypertension, diabetes, obesity, cardiovascular disease, and kidney disease NHANES-III showed that a serum urate level in excess of 6 mg/dL was an independent risk factor for coronary artery disease and that a serum urate level above 7 mg/dL was an independent risk factor for stroke

Question 38

what is metabolic syndrome? how is related to gout?

Answer 38

metabolic syndrome is a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes these conditions include increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels 86% of gout patients meet the criteria for metabolic syndrome

Question 39

how is chronic kidney disease and gout related?

Answer 39

men are 2 times more likely and women are 5.8 times more likely to develop end stage renal disease if they have gout

Question 40

what are the steps that lead to acute gout?

Answer 40

1. MSU crystals are phagocytosed by leukocytes and also interact with membrane receptors and signaling molecules 2. fusion of vacuolar and lysosomal membranes 3. phagolysosome rupture, activation of inflammasomes in cytoplasm of macrophage 4. cleavage of pro-IL-1 signaling, transcription, and synthesis of mediators inside macrophage 5. release of multiple pro inflammatory mediators from the macrophage 6. inflammation

Question 41

how do you treat acute gout?

Answer 41

corticosteroids, NSAIDs or colchicine

Question 42

how do you treat chronic gout long term?

Answer 42

1. Allopurinol 2. Febuxostat 3. Probenecid 4. Pegloticase 5. Lesinurad ACP recommends against initiating longterm urate-lowering therapy in most patients after a first gout attack or in patients with infrequent attacks --> only start if there's more than 2 attacks per year

Question 43

what diet changes can be made for gout?

Answer 43

1. weight loss 2. avoid alcohol 3. avoid sugar sweetened drink 4. avoid heavy meals and excessive meat and seafood 5. low fat dairy products 6. cherries 7. fruit and vitamin C 8. high fiber diet

Question 44

what does CPPD arthritis stand for?

Answer 44

calcium pyrophosphate dihydrate crystals aka pseudo gout!

Question 45

what are the types of psuedo gout?

Answer 45

type A = pseudogout type B = pseudo-rheumatoid arthritis type C = pseudo-osteoarthritis’ type D = without inflammation type E = asymptomatic type F = psuedoneuropathic

Question 46

what is CPPD?

Answer 46

CPPD covers all clinical manifestations of CPP deposition; it's an umbrella term

Question 47

what is acute CPPD arthritis?

Answer 47

monoarticular arthritis of over the age of 65 knee, wrist and shoulder

Question 48

what is chronic CPPD arthritis?

Answer 48

chronic oligoarthritis or polyarthritis inflammatory symptoms and signs occasional systemic upset (with elevation of CRP and ESR)

Question 49

how do you diagnose CPPD?

Answer 49

diagnosis of CPPD is by identification of characteristic CPP crystals in synovial fluid the crystals are parallelepipedic, predominantly intracellular crystals with absent or weak positive birefringence

Question 50

what are the radiological findings of CPPD?

Answer 50

radiographic chondrocalcinosis = deposits of calcium in the joint this supports the diagnosis of CPPD, but its absence does not exclude it

Question 51

what are the ultrasound findings of CPPD?

Answer 51

1. thin hyperechoic bands within hyaline cartilage | 2. hyperechoic sparkling spots in fibrocartilage

Question 52

what are the comorbidities of CPPD?

Answer 52

1. OA 2. metabolic disease 2. rare familial predisposition

Question 53

how do you decide how to treat CPPD?

Answer 53

nonpharmacological and pharmacological modalities should be tailored according to clinical features, general risk factors and predisposing metabolic disorders

Question 54

how do you treat acute CPPD?

Answer 54

1. Ice or cooling packs 2. Temporary rest 3. Joint aspiration 4. Intra-articular injection of long-acting GCS 5. NSAIDs 6. low dose oral colchicine

Question 55

how do you treat chronic CPPD?

Answer 55

1. Oral NSAID (plus gastroprotective treatment if indicated) 2. Colchicine (0.5–1.0 mg daily) 3. Low-dose corticosteroid 4. Methotrexate 5. Hydroxychloroquine

Question 56

what is the connection between OA and CPPD?

Answer 56

OA is causing cartilage damage age, hereditary factors or metabolic disease are causing crystal deposition which then causes cartilage damage as well so it's an amplification look for calcium pyrophosphate deposition and OA!

Question 57

how do you treat CPPD?

Answer 57

no treatment modifies CPP crystal formation or dissolution no treatment is required for asymptomatic CC

Question 58

what are BCP crystals?

Answer 58

basic crystal phosphate arthritis associated with OA looks like a red skin spot

Question 59

what is acute periarthritis?

Answer 59

an acutely painful monoarticular condition characterized by the juxta-articular deposition of calcium hydroxyapatite crystals and local inflammation.

Question 60

how do you treat acute periarthritis?

Answer 60

1. NSAIDS 2. colchicine aspiration and irrigation of the joint corticosteroid use is controversial

Question 61

what is chronic periarthritis?

Answer 61

a condition that involves painful swelling around joints it's known as a calcium crystal disease because the pain is caused by crystals of the mineral calcium rubbing against soft tissue inside the body.

Question 62

how do you treat chronic periarthritis?

Answer 62

1. ultrasound 2. disodium ethylenediaminetetraacetic acid -- can improve shoulder function and pain levels and decrease calcifications 3. arthroscopic or Surgical removal

Question 63

what is Milwaukee shoulder?

Answer 63

a destructive shoulder arthropathy due to deposition of hydroxyapatite crystals often seen in old women acute shoulder pain and swelling identification of these crystals in synovial fluid is the cornerstone of diagnosis

Question 64

how do you treat Milwaukee shoulder?

Answer 64

1. analgesics and NSAIDs 2. repeated shoulder aspirations 3. decreased joint use 4. surgery is sometimes helpful 5. supra scapular nerve blocks

Question 65

what are depot corticosteroid crystals?

Answer 65

Most frequent during the first 8 hours after injection An infection, generally develops considerably more slowly Nonsteroidal antiinflammatory drugs Depot corticosteroid crystals have to be aspirated

Question 66

what are calcium oxalate crystals?

Answer 66

kidney stones!!! these crystals are made from oxalate — a substance found in foods like green, leafy vegetables — combined with calcium they can also be caused by high doses of vitamin C or consumption of high levels of fructose they look like square diamonds

Question 67

what are lipid crystals?

Answer 67

cholesterol crystals are most often seen as broad plates with a notched corner most patients have mono arthritis in the knee and the wrist (most common); polyarthritis is rare

Question 68

in which diseases are lipid crystals seen?

Answer 68

1. RA 2. gout 3. OA