Week 7 MSK and Pain Flashcards
Free sensory nerve endings that are present in most tissues of the body. Can be stimulated by thermal, chemical, or mechanical/physical means.
Nociceptor
Pain from a stimulus that is normally non-painful.
Example: A light feather touch (that should only produce sensation) causes pain.
Allodynia
An enhanced response to a stimulus that is normally painful.
Example: Feeling intense, excruciating pain when touching a recently burned area of skin. It’s normal to feel pain after a burn, but _________ causes your nervous system to overreact in response to something painful.
Hyperalgesia
A diminished experience of pain in response to a normally painful stimulus. Diminished sensitivity to stimulation that is normally not painful, also defined as a raised threshold to painful stimuli.
Example: Taking analgesics for pain, exercise-induced ______
Hypoalgesia
Unusual or pathological sensitivity of the skin or of a particular sense.
Example: Heightened sensitivity to touch, hearing, sight.
Hyperesthesia
Impaired or decreased tactile sensitivity
Example: Decreased sensitivity to touch, numbness
Hypoesthesia
Unpleasant abnormal sensation, whether spontaneous or evoked - means abnormal sensation
Dysesthesia
An osseous defect of the pars interarticularis, allows a vertebra to slide anteriorly in relation to the vertebra below, commonly occurring at L5-S1.
Spondylolisthesis
What are the 2 types of bone tissue? Which is more prevalent?
Compact bone (cortical bone) makes up 85% of bone tissue.
Spongy bone (cancellous bone) makes up 15% of bone tissue.
Both are present in every bone in the body.
Compact bone makes up 85% of the skeleton. It is highly organized, solid and extremely strong. The basic structural unit is the Haversian system, containing which 5 components?
- Haversian canal
- Concentric layers of bone matrix (lamellae)
- Tiny spaces (lacunae) between lamellae
- Bone cells (osteocytes) within lacunae
- Small channels or canals called canaliculi
In which bone tissue and compartment is red marrow found?
In spongy bone tissue.
Lamellae (layers on bone matrix) are arranged in plates/bars called trabeculae that branch and unite with one another to form an irregular meshwork. In spaces between trabeculae is red marrow
Long bones are made up of these 3 parts:
- Diaphysis (narrow tubular mid portion) consists of a shaft of thick, rigid compact bone that can tolerate bending forces.
- Metaphysis (broader neck)
- Epiphysis (broad end of long bone) the broadness allows weight-bearing to be distributed over a wide area.
This type of bone consists of two plates of compact bone that are nearly parallel, between these layers is spongy bone. Examples scapula and ribs.
Flat bones
These types of bones are often cuboidal, consisting of spongy bone covered by a thin layer of compact bone. Example: bones of wrist or ankle
Short bones
These types of bones have various shapes that include thick and thin segments. Thin part consists of two plates of compact bone surrounding spongy bone. Thick part consists of spongy bone surrounded by a layer of compact bone. Example: vertebrae, mandible, facial bones.
Irregular bones
|What do we call the process by which internal bone structure is maintained, by reabsorbing existing bone and synthesis of new bone to replace it?
Remodeling
What are the 3 phases of bone remodelling?
Phase I (Activation): a stimulus (hormone, med, vitamin, physical stressor) activates the cytokine system to form osteoclasts. Osteoclasts attach to bone matrix by structures called podosomes.
- Phase II (Digestion): Osteoclasts digest bone, releasing degraded bone product into vascular system (calcium and phosphorus), leaving behind a resorption cavity that follows longitudinal axis of Haversian system.
-Phase III (Formation): osteoblasts lining walls of resorptive cavity express osteoid and alkaline phosphatase, forming sites for calcium and phosphorus deposition. As osteoid mineralizes, new bone is formed in successive layers (lamellae) in compact bone are laid down until cavity is reduced.
Remodeling can heal microscopic bone injuries, but gross injuries (fractures/surgery) heal by the same stages as soft tissue injurie. Of course, the end product is bone tissue instead of scar tissue.
The stages of bone healing are:
-Inflammation or hematoma formation
-Procallus formation (I looked up what a procallus is as it isn’t in our texts and found that this is also hematoma formation)
-Callus formation (I looked this up too. Fibrocartilaginous tissue, like glue to hold everything in place while repair occurs.)
-Replacement by basic multicellular units of the callus with lamellar or trabecular bone
-Remodelling of the periostea and endosteal surface of the bone to the size and shape of the bone before injury.
How long does bone remodeling usually take?
3-6 months
What are some contributing factors to consider re: bone repair time frame?
- severity of injury
- type and amount of bone tissue needing replacement (spongy=faster
- the blood and oxygen supply at site
- presence of growth and thyroid hormones, insulin, vitamins, and nutrients
- the existence of systemic disease
- age of patient
What are the 3 types of nociceptive pain?
Somatic, visceral and referred
Describe the quality of nociceptive pain
Somatic pain: Sharp, well localized (esp fast pain from A-delta fibres). Dull, aching, throbbing, poor localized (from polymodal C fibre transmissions)
Visceral Pain: Poorly localized. Aching, gnawing, throbbing, or intermittent cramping quality. Often radiates or is referred
Referred Pain: Depends on area of referral. Burning, shooting, shock-like, or tingling
What are the 2 types of neuropathic pain?
Central and peripheral
What causes peripheral neuropathic pain and what is an example?
Caused by peripheral nerve lesions
Peripheral sensitization – increase in sensitivity and excitability of primary sensory neurons and cells in dorsal root ganglion
Ex. nerve entrapment, diabetic neuropathy, chronic pancreatitis
What causes central neuropathic pain and what is an example?
Caused by lesion or dysfunction of brain or spinal cord
Central sensitization – progressive repeated stimulation of group C neurons in the dorsal horn leads to increased sensitivity of central pain signalling neurons
-> pathological changes in the CNS -> persistent pain
Ex: brain or spinal cord trauma, tumours, multiple sclerosis, postherpetic neuralgia, phantom limb pain
Describe the usual stimuli for pain
Nociceptors are pain receptors. They are free nerve endings in the afferent PNS, their stimulation produces pain
What are the three types of stimuli that pain receptors can sense?
Nociceptors can sense different types of stimuli:
Mechanical (pressure or mechanical distortion)
Thermal (extreme temperatures)
Chemicals (acids or chemicals of inflammation)
What are the 4 phases of nociception?
Transduction, transmission, perception and modulation
Describe the afferent pathway
Afferent (Ascending) Pathways – conduction of pain impulses to brain
along A𝛿 and C fibres (these are the primary order neurons)
-> dorsal horn of spinal cord, where synapse with excitatory or inhibitory interneurons (second order neurons)
->2 lateral spinothalamic tracts -> brain where they synapse with third-order neurons called projection neurons
-> connections with the reticular formation, hypothalamus, thalamus (major relay station of sensory information) and the limbic system.
Differentiate between A𝛿 and C fibres, specifically think about myelination and type of pain transmitted.
A𝛿 fibres: larger myelinated fibres; rapidly transmit sharp, well-localized “fast” pain sensations (ex. burn or pinprick on skin). Activation causes spinal reflex withdrawal of affected body part before pain sensation is perceived
C fibres: most numerous; smaller and unmyelinated; located in muscle, tendons, body organs, skin. Slowly transmit dull, aching, burning sensations that are poorly localized and often constant
Interpretive centres:
The quality of pain associated with nociceptive and neuropathic pain
Nociceptive: Pain associated transmitted via unmyelinated C fibres and myelinated A delta
Neuropathic: Peripheral and Central
After the afferent pathway the impulse enters the interpretive centers. What happens here?
1) somatosensory cortex for location and intensity of pain
2) Other areas of the brain for an integrated response to pain
Pain Matrix:
Sensory-discriminative system: From the somatosensory cortex.
Responsible for the identifying the presence, character, location, and intensity of pain
Affective-motivational system: From the reticular formation, limbic system, and brainstem.Determines a person’s conditioned avoidance behaviours and emotional responses to pain
Cognitive-evaluation system: From the cerebral cortex. Individual’s learned behaviour concerning the experience of pain Can modulate perception of pain
Describe the efferent pathway
Efferent (Descending) Pathways - inhibit or facilitate pain
Brain stimulates the periaqueductal grey matter (PAG) and the rostral ventral medulla (RVM) in the midbrain -> stimulates efferent pathways which inhibit afferent pain signals in the dorsal horn of the spinal cord
The RVM stimulates efferent pathways that facilitate or inhibit pain
Match the joint type to the degree of movement:
- synovial
- fibrous
- cartilaginous
A. Generally do not move
B. Allow some movement
C. Freely moveable
- Synovial – C. Freely moveable
- Fibrous – A. generally do not move
- Cartilaginous – B. Allow some movement
What does a fibrous joint connect? What is another name for a fibrous joint?
A fibrous joint connects bone directly to bone. Can also be known as synarthrosis or fixed joints.
Match the three types of fibrous joints with their examples
- Suture Fibrous Joint
- Syndesmotic fibrous joints
- Gomphosis fibrous joint
A. Flat bones of skull in young children
B. Teeth in maxilla
C. Radius/ulna or tib/fib
Suture Fibrous Joint – A. Flat bones of skull in young children
Syndesmotic fibrous joints – C. Radius/ulna or tib/fib
Gomphosis fibrous joint – B. Teeth in maxilla
What are the key features of cartilaginous joints?
Allow some movement
Connect two bones with pad of cartilage
What are the two types of cartilaginous joints and examples of them?
Symphysis – fibro cartilage – ex. Symphysis pubis, intervertebral discs
Synchondrosis – hyaline cartilage – joints between ribs and sternum (costal cartilage)
What are the key features of synovial joints?
Most common
Allow wide range of movements – flexion/extension, abduction/adduction, rotation (axis)
Enclosed in joint (articular) capsule with synovial fluid
Match the 6 types of synovial joints with the appropriate examples
- Hinge joint
- Pivot joint
- Plane (gliding joint)
- Ball & socket joint
- Condyloid (ellipsoid joint)
- Saddle joints
A. Metacarpophalangeal joint
B. Elbow joint
C. Sternoclavicular joint
D. Distal radial-ulnar joint
E. glenohumeral joint
F. Carpal bones joints
- Hinge joint – B. Elbow joint
- Pivot joint – D. Distal radial-ulnar joint
- Plane (gliding joint) - F. Carpal bones joints
- Ball & socket joint - E. glenohumeral joint
- Condyloid (ellipsoid joint) - A. Metacarpophalangeal joint
- Saddle joints – C. Sternoclavicular joint
What are the four rotator cuff muscles?
Supraspinatus
Infraspinatus
Teres minor
Subscapularis
What are the origin (proximal attachment) and insertion (distal attachment) for the supraspinatus, one of the rotator cuff muscles?
Origin: Supraspinatus fossa of scapula and deep fascia
Insertion: Greater tubercle of humerus
What are the origin (proximal attachment) and insertion (distal attachment) for the infraspinatus, one of the rotator cuff muscles?
Origin: infraspinatus fossa of scapula and deep fascia
Insertion: Greater tubercle of humerus
What are the origin (proximal attachment) and insertion (distal attachment) for the teres minor, one of the rotator cuff muscles?
Origin: lateral border of scapula
Insertion: Greater tubercle of humerus
What are the origin (proximal attachment) and insertion (distal attachment) for the subscapularis, one of the rotator cuff muscles?
Origin: subscapular fossa of scapula
Insertion: Lesser tubercle of humerus
What are ligaments and tendons formed from? Describe general structure.
Primarily composed of types III, IV, V, and VI collagen and fibroblasts
* Collagen & fibroblasts form fascicles, multiple fascicles form tendon or ligament
Which of ligaments or tendons
1) has less organized fibroblasts
2) contain more elastin?
LIGAMENTS FOR BOTH:
Fibroblasts less organized than in tendons (in tendons, form parallel rows)
Fiberss in ligaments contains more elastin than tendons
Can tendons and ligaments withstand stretch or compression better
- Both L&T can withstand significant stretch but tend to buckle with compressive force
Fx of ligaments
Attach bone to bone, helping to form joints and stabilize them against excessive movement
What are fibroblasts in tendons called?
Tenocytes
2 main Fx’s of tendons?
1) Transfers forces from muscles to bone
2) acts as spring for muscles to provide stability during movement.
What are bursae? Are they inside or outside of joints?
= Small sacs lined with synovial membrane and filled with synovial fluid that are located between bony prominences and soft tissues such as tendons, muscles, and ligament
* Lie OUTSIDE the joints
Fx of bursae?
to separate, lubricate, and cushion these structures (bones, ligaments, tendons)
* When healthy, create a smooth, almost frictionless functional gliding surface making normal movement painless.
T/F you are born with all of your bursae and never grow more.
False - you can grow new ones!
* Can either be constant (those formed during embryological development) or “adventitious” (bursae that develop as a result of chronic friction and degeneration of fibrous tissue between adjacent structures)
Describe the structure of the joint capsule. What is it made of? What kinds of fibres? What else does it contain?
- Fibrous connective tissue that covers the ends of bones where they meet in a joint (A “sleeve” around the joint)
- Sharpey fibres firmly attach the proximal and distal capsule to the periosteum & ligaments and tendons may reinforce the capsule
- Composed of parallel, interlacing bundles of dense, which, fibrous tissue richly supplied with nerves, blood vessels, and lymph vessels
Fx of joint capsule
The joint capsule is vital to the function of synovial joints. It 1) seals the joint space, 2) provides passive stability by limiting movements 3) provides active stability via its proprioceptive nerve endings and 4) may form articular surfaces for the joint.
Nerves in and around the joint capsule are sensitive to rate and direction of motion, compression, tension, vibration, and pain
- Lined with synovial membrane, which makes synovial fluid
Structure of the synovial membrane. What part of the joint does it line?
- Smooth, delicate inner lining of the joint capsule found in the NONPARTICULAR portion of the synovial joint & any ligaments or tendons that traverse this cavity
- Composed of 2 layers: vascular subintima and thin cellular intima
- Vascular subintima merges with joint capsule
- Cellular intima = rows of synovial cells embedded in matrix and contains A cells (macrophages that ingest bacteria & debris) and B cells (fibroblasts, most numerous, secrete hyaluronate makes synovial fluid viscous)
- Rich supply of blood and lymph. Can repair rapidly.
Fx of synovial membrane
- Clears bacteria & debris
- Makes hyaluronate (part of synovial fluid)
What is synovial fluid? What is it composed of?
- Superfiltrated plasma from blood vessels
- Contains hyaluronic acid, which gives it important biomechanical properties
- Contains free-floating synovial cells & various leukocytes that phagocytose bacteria & debris
Function of synovial fluid
- Lubricates joint surfaces, nourishes pad of the articular cartilage, and covers the ends of the bones
What do you call the site at which tendons connect muscle to bone?
The enthesis
What 4 muscles comprise the “rotator cuff”
1) Supraspinatus
2) Infraspinatus
3) Tenes minor
4) Subscapularis
ACRONYM = SITS
Where do the rotator cuff muscles originate and attach to?
Generally: Scapula to humerus
More specifically…
ORIGIN:
1. Supraspinatus: originates in Supraspinous fossa of scapula and deep fascia
2. Infraspinatus Originates in Infraspinous fossa of scapula and deep fascia
3. Teres Minor : originates from Lateral border of scapula
4. Subscapularis : originates from Subscapular fossa of scapula
INSERTION:
1) 2) and 3) insert at greater tuberosity of humerus. 4) inserts at lesser tuberosity of the humerus
**the term “spinatus” is referring to the spine of the scapula (the sticky outy linear part of bone that comes off the scapula). So “supra” means above this, and “infra” means below this.
WHat is the action (of the arm at the shoulder) that each of the rotation cuff muscles is responsible for?
1) Supraspinatus: ABduction until 15 degrees (then deltoid takes over)
2) Infraspinatus: external (lateral) rotation
3) Teres minus: external (lateral) rotation and ADDuction
4) Subscapularis: internal rotation (medial) and ADDuction
What is the general function of the rotator cuff?
Dynamic Shoulder stability (hold humerus in glenoid fossa while the arm moves around)
(The shoulder has HIGH mobility but LOW stability due to how the humerus head only sits partially in the glenoid fossa at any one time)
What is the largest and strongest muscle of the rotator cuff?
The subscapularis
Who is most likely to get intervertebral disc herniation?
One of the most common causes of working age individuals getting spinal surgery.
High occurrence in men
Highest occurrence is in men aged 30 to 50 years.
Risk factors are repeated lifting, physically demanding jobs, weight-bearing sports and light weightlifting.
What areas of the spine do you most often see disc herniation?
Most affected lumbosacral discs are L4-L5 and L5-S1.
The most affected cervical region is C5-C6 and C6-C7.
Lumbar disc herniation is more common than cervical disc herniation.
What exactly is happening with disc herniation?
It is caused by the displacement of the nucleus pulposus or annulus fibrosus beyond the intervertebral disc space.
The nucleus pulposus is hydrated and acts a “shock absorber” by compressing when lifting a load and relaxing when load is removed.
With age nucleus pulposus weakens, becomes less dehydrated and more gelatinous –> more of the compression forces transferred to the annulus fibrosus. Overtime, the compression-relaxation cycle causes peripheral tears of the annulus fibrosus. The tear allows the nucleus pulposus to bulge and protrude through the annulus fibrosus and this can compress the nerve root.
What is the annulus fibrosis?
The annulus fibrosus is the strong wrapping that makes up the outside portion of the intervertebral disc. Its job is to contain and protect the soft material located in the center of the disc. This soft center is called the nucleus pulposus.
Most common causes of disc herniation?
Most commn = degenerative process as we age
2nd most common = trauma
In which direction does the herniation most often occur?
Most disc herniations occur in the posteolateral direction where the annulous fibrous is thinner and is not well supported by the anterior or posterior longitudinal ligaments (I think posterolateral means back toward the spinal cord and off to the side a bit)
What causes the pain in disc herniation?
The combination of nerve root compression and release of local inflammatory cytokines causes localized back pain.
What is cauda equina syndrome?
Cauda equina syndrome is a condition that occurs when the bundle of nerves below the end of the spinal cord known as the cauda equina is damaged. Signs and symptoms include low back pain, pain that radiates down the leg, numbness around the anus, and loss of bowel or bladder control. Onset may be rapid or gradual.
Herniation in what area could lead to cauda equina syndrome
Multiple nerve root compressions may be found at the L5-S1 level affecting the cauda equina and leading to the cauda equina syndrome.
Is aggressive treatment usually necessary for herniated discs? What are the usual treatments?
“Over 85% of patients with symptoms associated with an acute herniated disc will resolve within 8 to 12 weeks without any specific treatments.”
Most herniated disc resolve on their own and do not require surgery.
Conservative treatments include NSAIDs, acetaminophen, therapeutic massage and physical therapy.
May require neurosurgery consultation.
S&S of disc herniation
The location and size of the herniation into the spinal canal and amount of space in the canal determine clinical signs. It causes radiculopathy or pinched nerve - injury to nerve roots in the area where they leave the spine.
Radiation of the pain follows distribution of the compressed nerve root. Lumbosacral area causes pain in the sacroiliac joint, buttocks, hip, posterior thigh, and leg. Cervical disc herniation causes shoulder and upper limb pain and hand. Pain increases with movements and straining. Range of motion is decreased in the lumbar spine or neck.
Numbness, tingling, decreased sensation, decreased range of motion and motor weakness of the extremities may occur along the path of the nerve root.
What diagnostic might we do for herniated disc? What is the significant of leg raise tests here? Which leg raise tests is highly SPECIFIC for herniation? Which is more SENSITIVE?
X-rays, CT-scans and MRI.
MRI is the most sensitive and preferred method if disc herniation is suspected.
CT myelography can be used to visualize herniated discs if patients are unable to do MRI.
The Straight Leg Raise (SLR) test is a commonly used test to identify an impairment in disc pathology or nerve root irritation. It have also specific importance in detecting disc herniation and neural compression.
The straight leg raise test is more sensitive but less specific than the contralateral straight leg raise for the diagnosis of radiculopathy due to disc herniation [40]. It is most helpful in the evaluation of radiculopathy at the L5 and S1 levels. Contralateral leg raise test is relatively specific for radiculopathy due to disc herniation, but has poor sensitivity
Straight leg test - how is it done?
The straight leg raise test: With the patient lying supine, the examiner slowly elevates the patient’s leg at an increasing angle, while keeping the leg straight at the knee joint (movement must be PASSIVE). The test is positive if it reproduces the patient’s typical pain and paraesthesia.
The contralateral (crossed) straight leg raise test: As in the straight leg raise test, the patient is lying supine, and the examiner elevates the asymptomatic leg. The test is positive if the maneuver reproduces the patient’s typical pain and paraesthesia.
What is radiculopathy?
= pinched nerve in the spine
Are men or women most likely to get fibromyalgia?
80-90% of cases are women!
What is fibromyalgia?
Chronic musculoskeletal syndrome characterized by diffuse pain, fatigue, increased sensitivity to touch, absence of systemic or localized inflammation, and the presence of fatigue and nonrestorative sleep, anxiety, depression.
Can coincide with autoimmune diseases such as lupus and IBS
At what age does fibromyalgia usually present?
30-50
What do we know about the cause of fibromyalgia?
Genetic factors have a role- individuals with family members with FM have an increased risk
Alterations in genes affecting serotonin, catecholamines, and dopamine.
External stressors such as infection, psychosocial stress, physical or emotional trauma are proposed mechanisms that may precipitate FM.
There is a lot more to discover about FM.
S&S of fibromyalgia
Most prominent symptom is diffuse persistent pain- present for more than 3 months.
Pain often begins in one location such as neck and shoulders and then becomes more generalized.
Describe pain as burning or gnawing.
- Profound fatigue
- Headaches
- Memory loss
- Poor sleep
Diagnosis of fibromyalgia?
Need to rule out other disorders such as rheumatic disorders.
Diagnosis is based on assessment and the Canadian guidelines for the diagnosis and management of fibromyalgia syndrome: pain that has been present at similar level for at least 3 months with insidious onset, usually localized to a particular one area, pain might be neuropathic in nature, there is no other underlying pathology to explain the pain. AND other associated symptoms: fatigue, nonrestorative sleep, cognitive dysfunction, changes in mood.
There is no other testing for fibromyalgia.
Treatment and patient teaching for fibromyalgia?
Should be individualized
Mind-body interventions
Movement therapies
Relaxation techniques
Medication: NSAIDs, opioids, cannabinoids, antidepressants. And anticonvulsants.
Patient teaching: not caused by infection, not deforming, or deteriorating, not life threatening, assist the individual to use aerobic exercises to reduce stress and increase rapid eye movement, stress that illness is real and not imagined, discuss the role of sleep disturbances and the relationship of neurohormones to pain, fatigue, abnormal sleep, and mood, and that reassure that although the cause is unknown some information is known about the physiological changes responsible for symptoms.
WHat is gout?
a type of acute inflammatory arthritis of the joint, caused by uric acid crystals depositing in the joints and bones.
Are men or women most often affected by gout? WHat age group?
Men
Ages 30 to 60 yrs most common but also common in elderly
*Rare in children
At what phase of life are women most susceptible to gout?
Women become increasingly susceptible to gout after menopause; rare premenopausal (estrogen promotes uric acid excretion).
What is uric acid?
Uric acid is a natural byproduct of purine. Purines are produced in the body and also found in certain foods/drinks. Normally, uric acid is excreted out by kidneys in the form of urate.
Patho of gout
Closely linked to purine metabolism and kidney function.
If there is an imbalance between uric acid production and excretion, hyperuricemia may result.
Uric acid crystals begin to form on joints and bones.
Macrophages phagocytize these crystals, which initiates the inflammatory cascade → results in an acute gout attack.
Chronic hyperuricemia occurs when the kidneys are unable to effectively excrete uric acid.
What predisposes a person to gout?
Chronic conditions: Hyperuricemia, kidney disease, hypertension, diabetes mellitus, ischemic cardiovascular disease, hyperlipidemia, obesity.
Genetics → about 10% of population has a predisposing factor for excessive uric acid production.
Gender → men older than 30 years.
Medications that inhibit uric acid excretion by kidneys. E.g., Diuretics, ASA, nicotinic acid, ethambutol
High-purine diet
High intake of alcohol (especially beer)
High intake of meat and certain seafoods (e.g., shrimp & oily fish).
Describe the phases of gout. What forms when it becomes chronic/untreated?
1) High uric acid levels: Uric acid is building up in blood and starting to form crystals on joints. Asymptomatic.
2) Acute gouty arthritis: Acute attack exhibiting severe pain, redness, and swelling of a joint, which may last from days to weeks, even if left untreated.
3) Intercritical gout: Period without flares.
4) Chronic/tophaceous gout: Gout pain is frequent (3+ attacks per year) and tophi form in joints and soft tissues, potentially causing deformity and disability of joints.
If left untreated, will grout attacks stop on their own?
Without treatment, gout attacks increase in length and frequency, and can eventually become chronic.
______ is the most common aggravating factor of acute gouty arthritis.
Trauma
Describe the classic presentation of gout. S&S. What joint is most often affected?
Erythema, swelling, warmth, and/or pain in the joint.
Reduced joint range of motion.
Monoarticular (affects one joint). Often big toe.
Pain is likely to be most severe during the first 12-24 hours.
Hx of severe joint pain with inflammation in other joints, followed by pain-free episodes.
Other possible signs
Tophi are seen from untreated gout.
Fever may be present during acute stage (not always).
Do tophi only present after multiple gout attacks have taken place? WHy is it important to keep an eye out for them?
Deposits of uric acid crystals or tophi in joints and other tissues can be present years before an acute gout attack occurs.
Timely identification allows for early treatment and ongoing support.
What is the definitive test for gout?
Joint fluid aspiration
Gold standard in diagnosing gout.
Inspect fluid with a polarized light microscopy to identify uric acid crystals.
What laboratory findings will you see with gout?
WBC → Elevated.
ESR → Elevated.
CRP → elevated.
Serum uric acid level: Uric acid >404.46 umol/L.
Rheumatoid factor (RF) titre.
T/F serum uric acid level will always be elevated during a gout attack
F: Serum uric acid level may be normal during acute attacks. Perform test at least 2 weeks after acute attack (or when flare has resolved).
Treatment of grout?
Goal during a gout attack: Relieving pain and inflammation.
General Interventions
Rest the joint.
Avoid heavy lifting or weight-bearing activities on that joint.
Cold therapy on affected joint to relieve pain and inflammation.
Discontinue ASA, if using.
Pharmacology
Analgesia for symptom control.
NSAIDs – most effective if started within 48 hrs of presenting symptoms.
Colchicine – an option for those who cannot take NSAIDs. However, colchicine comes with side effects that may not be tolerated.
Corticosteroids – for patients who cannot tolerate either NSAIDs or colchicine
Patient teaching for gout
Patient Teaching
Increase fluid intake → aim for 8+ glasses of water daily.
Avoid alcohol intake.
Avoid excessive meat and seafood products that trigger flares.
Medication education and compliance → taking medication can be effective in preventing chronic gout stage.
What medications may be used long term in gout for prevention?
For uric acid hypersecretion → need long-term therapy to decrease uric acid production.
Allopurinol (first line of tx).
For reduced excretion of uric acid
Consider probenecid.
Encourage increased fluid intake.
If clients have 3 or more attacks per year, consider long-term therapy:
low dose of NSAIDs, or
Allopurinol
What is septic arthiritis? is it urgent?
Septic arthritis is a potentially fatal infection of the joint space; usually bacterial, but occasionally fungal, viral, or mycobacterial.
*Surgical emergency → The affected joint can be destroyed within 24 hours.
Who most often gets septic arthritis? Why has incidence increased in recent times?
More prevalent in children and the elderly.
Children: 5-12 cases per 1,000
Peaks around age 2-3 years.
More prevalent in males.
Incidences of septic arthritis has increased in recent years, due to:
Increased prosthetic joint surgeries.
Aging population.
Increased use of immunosuppressive therapy.
What are the ways that a joint gets infected (4)?
Primary routes by which pathogens accumulate in joints:
1) Hematogenously (systemic infection)
2) Neighbouring soft tissue sepsis (e.g., osteomyelitis).
3) Trauma – direct inoculation of bacteria (e.g., open fracture, animal bite)
4)Iatrogenic events (e.g., joint surgery, arthrocentesis, steroid injections).
Primary causative agents of septic arthritis
Staphylococcus aureus → most common; any age group.
Group A streptococcus → from respiratory infection; usually children.
Neisseria gonorrhoeae → STI; mainly young adults
Methicillin-resistant S. aureus
Risk factors for septic arthritis
Underlying joint disease (rheumatoid arthritis, osteoarthritis, gout).
Recent joint surgery (prosthetic joints)
Chronic diseases: diabetes mellitus, leukemia, cirrhosis, granulomatous diseases, cancer.
Immunosuppressive therapy and/or glucocorticoids.
Hemodialysis.
HIV.
Intravenous drug abuse.
Cutaneous ulcers.
Previous intra-articular corticoid injections.
Low socioeconomic status.
Patho of septic arthritis - how does it lead to necrosis of the joint?
Bacterial invasion into synovium and joint space via bloodstream, nearby infection, or directly.
Bacteria release toxins (e.g., chondrocyte proteases) that destroy articular cartilage.
Macrophages phagocytose bacteria, while releasing inflammatory cytokines which also mediate joint destruction.
Mast cells release histamine → causes vasodilation & increased vascular permeability → blood enters area (red, swollen, warm joint)
Increased intra-articular pressure due to fluid leaking out of capillaries → compresses & interrupts blood supply to the joint → necrosis of joint.
Potential complications of septic arthritis?
Osteomyelitis
Chronic pain
Osteonecrosis
Length discrepancies
Sepsis
Death
Aggressive physiotherapy after the acute phase is necessary to restore joint function.
S&S of septic arthritis?
Erythema, swelling, warmth, and/or pain in the joint. Reduced joint range of motion. (these are same as gout)
“Pseudoparalysis” – or marked guarding to motion of the joint; inability to bear weight.
Children appear quite ill: malaise, anorexia.
Typically monoarticular, but assess for polyarticular septic arthritis. - More than one joint is affected in 22% of cases.
Note: Fever is not a reliable indicator of an infected joint (a mild fever may be present).
**Symptoms usually present for <2 weeks
What joints are most commonly affected by septic arthritis in adults vs children?
Knee (adults)
Hip (children)
Ankles
Elbows
How do we diagnose septic arthritis?
What might we see in labs?
Definitive Diagnosis Test
Joint fluid aspiration
Presence of bacteria in synovial fluid.
May have elevated WBC in SF.
Laboratory Findings
WBC → elevated.
ESR → elevated.
CRP → elevated.
Note: the absence of elevated ESR, CRP or WBC does not exclude dx of septic arthritis.
Blood Cultures
Isolate causative bacteria to tailor antibiotic treatment.
Note: Blood cultures are only positive in 30-40% of cases.
What are the Kosher criteria for diagnosing septic arthritis?
There is a greater than 90% chance of a septic joint if 3 of the 5 following criteria are met:
WBC greater than 12 x 109/L
Inability to bear weight on the joint
Fever greater than 38.5C
ESR greater than 40mm/hr
CRP greater than 0.190 mcmol/L
