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
How do we treat septic arthritis?
Surgical emergency
Quick diagnosis and treatment is essential to reduce morbidity and mortality.
Referral: If septic arthritis is suspected, immediate referral to an orthopedic surgeon is needed.
Antibiotic Treatment → Prompt antibiotic treatment. Start on broad-spectrum antibiotics. Switch to specific antibiotics when culture results return.
Joint Drainage → Prompt removal of any purulent material from joint space; achieved either surgically (open drainage) or via closed needle aspiration (arthrocentesis).
Analgesia → NSAIDs, acetaminophen
Splints to maintain correct positioning.
During the acute phase of infection, optimal positioning of joint is essential to avoid subsequent deformities and contractures.
Isotonic exercise → must be initiated to prevent muscular atrophy during the acute phase.
Physiotherapy → after the acute phase, early physiotherapy and mobilization is important to ensure optimal recovery of joint.
What are the three main muscular compartments of the thigh?
Anterior (extensor)
Medial (adductor)
Posterior (flexor)
Each component contains its own muscles, blood vessels and nerves.
Which muscular compartment of the thigh is the largest? What do the muscles here do?
Anterior compartment is the largest. Muscles are flexors of the hip and extensors of the knee.
What is the only muscle that attaches to the vertebral column, pelvis and femur? It is in the anterior compartment of the thigh and is the major flexor of the thigh at the hip joint. Also, flexor of lumbar vertebral column and postural muscle, helping to maintain lumbar lordosis.
The Iliopsoas (including the Psoas major and the Iliacus)
One of the anterior compartment thigh muscles is the longest muscle in the body. It originates at the anterior superior iliac spine, with insertion at the medial surface of tibia, travelling diagonally across the thigh, lateral to medial. Flex both hip and thigh, when both sides work together, they bring the legs into the cross-legged sitting position. Which muscle is this?
Sartorius
The Vastus lateralis, vastus intermedius, vastus medialis and rectus femoris are the four components of which muscle group in the anterior thigh?
Quadriceps Femoris. Together these are among the largest and most powerful muscles in the body, they act on both the hip and knee joints.
Describe the Quadriceps tendon, where does it arise from and where does it end?
The tendon of all four of the Quadricep Femoris muscles unites to form the quadriceps tendon (which then envelopes the patella, continues as the patellar ligament, with insertion on the tibial tuberosity.) Medical and Lateral vastus muscles also attach independently to the patella, increasing patellar stability and centering the patella.
Which nerve supplies the Quadriceps muscles?
Femoral Nerve (L2-L4)
To recap, what are the three major muscles of the anterior compartment of the thigh?
Iliopsoas (Psoas Major, Iliacus)
Sartorius
Quadriceps (Vastus lateralis, vastus intermedius, vastus medialis and rectus femoris)
What is the main function of the muscles in the medial compartment of the thigh?
Adduction
What are the names of the 5 muscles in the medial compartment of the thigh?
Adductor magnus, adductor longus, adductor brevis, obturator externus, gracilis
The “hamstring” is part of which muscle in the medial compartment of the thigh?
The adductor magnus. This is the largest muscle in the medial compartment, adducts thigh, composed of two parts: adductor (adducts) and hamstring (extends thigh)
Which muscle in the medial compartment of the thigh is long, thin and medial, with functions of adducting thigh at the hip, flexing leg at knee and helping with medial rotation? This muscle joins the sartorius and semi tendinosis in forming the Pes Anserinus tendon
Gracilis
Which muscle in the medial compartment of the thigh is short and deep, origin at margin of obturator foramen and insertion at posterior aspect of greater trochanter? This muscle laterally rotates the thigh and steadies the head of the femur.
Obturator Externus
Which nerve primarily innervates the medial compartment of the thigh?
Obturator nerve (L2-L4)
(Exception: hamstring of adductor magnus is innervated by the tibial part of the sciatic nerve)
What are the 3 muscles of the posterior compartment of the thigh? What are these muscles collectively called?
Semitendinosus, semimembranosus, biceps femoris
Collectively called the hamstrings (except for the short head of the biceps femoris muscle)
These muscles generally originate on the ischial tuberosity, insert on bones of the leg and extend the hip and flex the knee.
Which posterior thigh muscle is half muscular belly and half cord-like tendon?
Semitendinosus
This muscle joins the sartorius and gracilis in forming the Pes Anserinus tendon
Semimembranosus
This muscle in the posterior compartment of the thigh has two heads
Biceps femoris – short head and long head
Identify the innervation of the posterior compartment of the thigh
Sciatic Nerve (L5-S2) - tibial division for all, except the short head of the biceps femoris = fibular division of sciatic nerve
Where is the anterior talofibular ligament?
Anterior distal tibia and fibula, runs obliquely
What is a sprain?
Ligament tear
Which type of ankle sprain is most common and what often causes it?
Lateral ankle sprain is most common and usually involves the ATFL. Ankle sprains are typically caused by inversion injuries – when the foot is plantarflexed – places stress on the components of the lateral collateral ligaments
What are the common S/S of a sprain of the anterior talofibular ligament?
-pain over lateral ankle
-swelling hours after inciting event
-inability to ambulate
What special test can be done to confirm sprain of the anterior talofibular ligament
Anterior drawer test: tibia is held steady while the heel is pulled anteriorly with the foot in about 10-20 degrees of plantarflexion. This will confirm the injury to the ATFL if the translation (laxity) of the foot anteriorly is excessive compared with that of the uninjured ankle.
Are males or females more likely to be diagnosed with Ankylosing Spondylitis?
Men are three times more likely
What is the peak age of incidence of Ankylosing Spondylitis?
Age 20 peak start of symptoms. Although often delay in diagnosis
Describe basic Ankylosing Spondylitis patho
chronic systemic autoimmune inflammatory disease, characterized by stiffening/fusion (ankylosis) of primarily spine and sacroiliac joints, with excessive bone formation. Can also affect large peripheral joints
Inflammation occurs at entheses (insertion site of ligaments and tendons on bones)
Inflammatory cells invade the joint and erode the bone and fibrocartilage of the joints. Body then tries to repair the area and forms fibrous scar tissue. This is then replaced by ossified scar tissue, causing fusion
What spine changes are likely with Ankylosing Spondylitis?
Fusion
“Bamboo spine”
Lumbar lordosis and kyphosis
What classically relieves pain related to Ankylosing Spondylitis?
Pain is usually improved by activity and aggravated by rest
Common S/S of Ankylosing Spondylitis?
Gradual onset of low back pain and stiffness during early 20’s
Pain starts as insidious, becomes persistent. Worse with prolonged rest, improved by physical activity
SI joint pain
Joint pain occurring for more than 3 months with morning stiffness
Dactylitis (sausage digits of the fingers/toes)
Enthesitis (inflammation/pain at the insertion site of the tendon or ligament to the bone
What is treatment for Ankylosing Spondylitis?
Referral to rheumatology
Education about the disease
Continuous physical therapy program to maintain skeletal mobility and prevent progression of contractures
NSAIDs/ analgesia medications to provide symptom relief and facilitate exercise
Biological response modifying agents. Ex. Certolizumab, golimumab, rituximab
Possible surgical procedures: osteomy, total hip replacement, cervical spinal fusion
What is the most common sign of heel pain in the outpatient setting?
Plantar Fasciitis
What is the patho of Plantar Fasciitis?
Shortening or contracture of calf muscles and plantar fascia
the result of collagen degeneration of the plantar fascia at the origin, the calcaneal tuberosity of the heel
What are some risk factors for Plantar Fasciitis?
Risk factors for shortened calf muscles include a sedentary lifestyle, occupations requiring sitting, very high or low arches in the feet, and chronic wearing of high-heel shoes
Common among runners and dancers and may occur in people whose occupations involve standing or walking on hard surfaces for prolonged periods
Also associated with obesity, RA, reactive arthritis and psoriatic arthritis
S/S of Plantar Fasciitis
Pain at bottom of heel. It is often worse when pushing off of the heel (the propulsive phase of gait) and after periods of rest. Some patients describe burning or sticking pain along the plantar medial border of the foot when walking.
Dorsiflexion of patient’s pedal phalanges
How is Plantar Fasciitis diagnosed?
Confirm the diagnosis by reproducing pain with calcaneal pressure exerted by the thumb during dorsiflexion
Outline treatments for plantar fasciitis
Treatment involves calf muscle and plantar soft-tissue foot-stretching exercises, night splints, orthotics, and shoes with appropriate heel elevation
What is the location of a radial head fracture?
Proximal radius
What are S/S of a radial head fracture?
typically present within 48 hrs of fall onto outstretched (FOOSH) hand or direct elbow trauma
Pain, tenderness or swelling over the lateral elbow or decreased elbow motion following any type of trauma
Joint tenderness over the radial head
What is the location of a distal radius fracture? What are the two types?
Distal radius
Colles Fracture (extension) – dorsal displacement of distal radius fragment
Smith Fracture (flexion) – palmar displacement of distal radius fragment
What are S/S of a distal radius fracture?
Most common mechanism is FOOSH injury
Colles’ fall with hand outward, Smith’s fall with hand inward
Pain of wrist and possibly edema and deformity
This muscle of the rotator cuff abducts the shoulder.
Supraspinatus.
This muscle of the rotator cuff laterally/externally rotates the shoulder.
Infraspinatus.
This muscle of the rotator cuff medially/internally rotates and adducts the shoulder.
Subscapularis.
This muscle of the rotator cuff laterally/externally rotates the shoulder.
Teres Minor.
What are the 4 tendons of the rotator cuff?
Which is most vulnerable to injury?
Supraspinatus tendon. Most vulnerable to injury
Infraspinatus tendon
Subscapularis tendon
Teres Minor tendon
What are the 3 bursae of the shoulder?
Subacromial
Subdeltoid
Subscapular
Nerves that innervate most of the shoulder muscles and all the muscles of the upper limb arise from the ____________.
Brachial plexus.
The deltoid muscle has 3 parts. What are they, and what action does each have on shoulder movement?
Anterior part: Flexes and medially rotates arm at shoulder
Middle part: Abducts arm at shoulder
Posterior part: Extends and laterally rotates arem at shoulder
What are teh 3 anterior muscles of the upper arm
What are the 3 anterior muscles of the upper arm?
What are their actions?
Biceps Brachii - Supinates flexed forearm; flexes forearm at elbow.
Brachialis - Flexes forearm at elbow in all position.
Coracobrachialis - Helps to flex and adduct arm at shoulder.
What are the 2 posterior muscles of the upper arm?
What are their actions?
Triceps brachii - Extends forearm at elbow’ is chief extensor of elbow; steadies head of abducted humerus (long head).
Anconeus - Assists triceps in extending elbow; abducts ulna during pronation.
The olecranon bursa is located posteriorly over the olecranon process of the ulna. Acute bursitis often presents with visible swelling, redness and warmth. Normally caused by trauma, infection or rheumatic disease specifically RA, gout.
How does bursitis here affect flexion and extension of the elbow?
Can fully extend without difficulty.
Full active or passive flexion of elbow is uncomfortable.
Scapulothoracic bursitis results from the mechanical pressure and friction between the superior-medial angle of the scapula and the adjacent ribs.
What are common complaints?
What are common aggravating activities?
What are some possible exam findings?
Pain and a “popping” sensation are typical complaints.
Aggravating activities include repetitive movements such as working overhead, reaching up and forward, or doing pushups.
Local tenderness and palpable crepitus are characteristic. An effusion or hemorrhage into the area may be seen on MRI.
Which demographic has the highest incidence of intervertebral disc herniation?
What are the common risk factors?
Men aged 30-50 years.
Common risk factors are repeated lifting, physically demanding jobs, weight-bearing sports and light weightlifting.
Advancing age is in itself a significant risk factor.
Which regions of the spine are most commonly affected by intervertebral herniated discs?
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.)
If multiple nerve root compressions occur at the L5-S1 level, what syndrome might occur?
Cauda equina syndrome.
“Over 85% of patients with symptoms associated with an acute herniated disc will resolve within 8 to 12 weeks without any specific treatments.”
Totes or nope?
Totes.
What are some symptoms you might see in a patient with acute herniated disc?
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.
How do you perform a straight leg-raise test?
What are you testing for?
The straight leg raise test: With the patient lying supine, the examiner slowly elevates the patient’s affected leg at an increasing angle, while keeping the leg straight at the knee joint. The test is positive if it reproduces the patient’s typical pain and paraesthesia.
You are testing for herniated disc in the lumbosacral region
Note: the test can be performed with the unaffected leg and is called the contralateral leg raise test. This test has a 90% specificity if positive.
What is the recommended treatment for herniated disc?
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 if ongoing or symptoms are not manageable.
What percentage of people with psoriasis will develop psoriatic arthritis?
10-30%
What are some predisposing factors or psoriatic arthritis?
Occurs equally in both biological sexes
Age (onset usually between 20-55 years of age)
Family history (40% of affected individuals have first degree relative with PsA)
Genetic predisposition
Psoriasis (especially those nail pitting or onycholysis). Majority present with psoriasis first.
Median time between joint disease diagnosis is 7-8 years after psoriasis onset, in some patients can be up to 40 years
Environmental triggers
Physical trauma
Infection
What are possible complications of psoriatic arthritis?
Cardiovascular disease, especially in those who aren’t on disease-modifying anti-rheumatic drugs (DMARDs)
Metabolic syndrome (hypertension, diabetes etc.)
Psychiatric morbidity – anxiety and depression
Non-alcoholic fatty liver
Anemia of chronic disease
What is the most common and mildest form of psoriatic arthritis (PsA)?
Asymmetric/Oligoarticular PsA
What is the least common and harshest form of psoriatic arthritis (PsA)?
Arthritis Mutilans/Destructive PsA
What are some of the physical findings you can expect to see in a patient who has psoriatic arthritis?
Decreased range of motion (ROM) in affected joints
Dermatological psoriasis (red plaques/silver scales)
Nail pitting, onycholysis and/or discoloration
Uveitis
Dactylitis (inflammation of fingers/toes “sausage” digits)
Enthesopathy (inflammation/pain at insertion site of the tendon or ligament to the bone) commonly seen in the Achilles tendon, plantar fascia, or tibial tuberosity
Tenosynovitis (inflammation of synovium)
Limp secondary to heel tenderness
What diagnostics would you consider to diagnose/rule out psoriatic arthritis?
Serum Bloodwork:
- Erythrocyte sedimentation rate (ESR) - elevated
- C-reactive protein (CRP) - elevated
- Leukocytosis
- Rheumatoid Factor (RF) - usually negative (positive in up to 15% of clients)
X-Rays of affected joint: shows joint erosion and classic feature of pencil-in-cup radiographic sign (DIP joint malformation)
If you have a patient with suspected psoriatic arthritis, early identification is necessary to prevent irreversible joint damage.
It may require systemic therapy and management typically done by _________ (who would you refer them to)?
Rheumatology.
What are common risk factors for gout?
Male
Increasing age
High alcohol intake
Red meat consumption
Fructose consumption
The following is the pathophysiology for which disorder?
“Uric acid (urate) is end product of purine catabolism. Humans do not possess the enzyme uricase to degrade urate crystals. Gout results from either over production or under excretion of uric acid.
At high concentrations, urate forms crystals which are deposited in connective tissues causing cellular injury and initiating the inflammatory response.”
Gout.
What are tophi?
What risk do they pose?
Tophi are uric acid deposits in the soft tissues. Strongly associated with causing destruction and deformity of the joint.
Patients with BLANKETY BLANK have 1000x greater risk of developing gout.
Kidney stones.
Acute gout typically affects one joint, but several can be involved. What are the most common sites?
Most common sites (in decreasing frequency): first metatarsophalangeal joint (big toe), instep of the foot, ankle, heel, knee, wrist, fingers, elbow
True or false?
Gout may also affect bursae?
True.
Most commonly affected bursae are in elbows, knees, Achilles.
True or false?
Diuretics are a first-choice treatments for gout.
False.
Diuretics are a common trigger.
Patients with gout should limit consumption of which food/drinks?
-Meats, especially organ meat.
-Seafood, especially shellfish, sardines and anchovies.
-ETOH, especially beer..
Intake of which food/drinks may reduce the risk of gout attacks?
-Coffee
-Vitamin C (500 mg/day)
- Low fat dairy (milk, yogurt)
-Tart cherries (not in pill form)
Lateral Epicondylitis is also known as _______.
Tennis elbow.
Medial Epicondylitis is also known as ________.
Golfer’s elbow.
The risk factors and pathophysiology for lateral epicondylitis (tennis elbow) and medial epicondylitis (golfer’s elbow) are similar.
Tennis elbow occurs as a result of injury to the extensor carpi radialis brevis (ECRB) tendon and forearm extensor muscles.
Golfer’s elbow occurs as a result of injury to pronator teres & flexor carpi radialis muscles.
How does pain present in each? (multiple answers)
Lateral epicondylitis (tennis elbow):
-painful to the outside of the elbow.
-pain with both passive and resisted wrist extension with elbow extended
-pain increases when lateral area is pressed or when grasping or twisting objects.
Medial epicondylitis (golfer’s elbow):
-pain to the inside of the elbow
-pain with both passive and resisted wrist flexion with elbow in full extension
-pain occurs on the ulnar side of the forearm, the wrist and occasionally the fingers
-stiffness of the elbow, weakness in the hand and the wrist and a numb or tingling feeling in the fingers (mostly ring and little finger)
-local tenderness over medial epicondyle and the conjoined tendon of the flexor group
What are some options for treating lateral epicondylitis (tennis elbow)?
Patient teaching (early symptoms):
-resting the elbow
-applying ice or heat several times a day for 1-2 weeks
-Stopping or changing activities that irritate tendon (also important for prevention)
NSAIDs (topical or oral) for pain control
Physio to strengthen and increase flexibility, change of movements
Counterforce brace
If condition gets worse consider:
-Corticosteroid injection
-Surgery (not done often)
What are some options for treating medial epicondylitis (golfer’s elbow)?
Same as lateral:
Patient teaching (early symptoms):
-resting the elbow
-applying ice or heat several times a day for 1-2 weeks
-Stopping or changing activities that irritate tendon (also important for prevention)
NSAIDs (topical or oral) for pain control
Physio to strengthen and increase flexibility, change of movements
Counterforce brace
If condition gets worse consider:
-Corticosteroid injection
-Surgery (not done often)
Mentioned additionally for lateral epicondylitis:
-Prolotherapy
-Eccentric exercises (no examples given)
-Extracorporeal shockwave therapy
-Needling
-Platelet-rich plasma (PRP)
-Autologous tenocyte injections
There are excitatory and inhibitory neurotransmitters involved in pain modulation. What do excitatory NTs do?
Pain “facilitators”- act to modulate control over transmission of pain impulses in periphery, spinal cord, and brain
Name the excitatory NTs involved in pain modulation
- Glutamate
- Substance P
- Histamine
- Prostaglandin
- Bradykinin
What excitatory NTs are released in response to peripheral tissue injury?
Prostaglandin, histamine, bradykinin
What excitatory NTs are released in response to chronic inflammatory lesions?
Lymphokines
There are excitatory and inhibitory neurotransmitters involved in pain modulation. What are the inhibitory NTs?
GABA, glycine
Norepi and serotonin play a role in pain inhibition of in the medulla, but can excited peripheral nerves
What are endogenous opioids? (definition)
Endogenous opioids (analgesics) are a family of morphine like neuropeptides that prevent the transmission of pain signals in the periphery, spinal cord, and brain.
Describe the mechanism of action of endogenous analgesics
Bind to opioid receptors (mu, kappa, delta)
Hinder ion channels to prevent release of excitatory NTS in the posterior horn of SC
In the midbrain, affect descending inhibitory pathways
In peripheral inflamed tissue, opioids are made and released from immune cells and active opioid receptors on sensory nerve terminals
Opioid receptors are widely distributed throughout the body and are responsible for sensations of well being and modulation of many physiologic processes
What is the most numerous of the natural opioids?
Enkephalins
What do enkephalins bind to?
Delta opioid receptors
Which of the natural opioids creates the greatest sense of excitement and substantial natural pain relief?
Endorphins (endogenous morphine)
What is the strongest of the endogenous opioids?
Dynorphins- play a role in neuropathic pain, mood disorders, and medication addition
What do endorphins bind to?
Mu
What do dynorphins bind to?
Kappa (firmly) to decrease pain signals
What do endomorphins bind to?
Mu receptors- strong pain relief effects
What is the only opioid receptor antagonist?
Naloxone
What does naloxone bind to?
Higher attraction for Mu receptors
*endorphins and endomorphins bind to mu receptors
What are endocannabinoids?
Made from phospholipids, classified as eicosanoids. Activate cannabinoid CB1 (in CNS) and CB2 (immune tissue and spleen) to modulate pain and other function (sleep, memory, appetite, stress, thermoregulation, addiction)
How do CB2 (cannabinoid) receptors decrease pain?
CB2 receptors decrease pain transmission by inhibiting release of excitatory neurotransmitters (in the spinal posterior horn, periaqueductal grey, thalamus, rostral ventromedial medulla, and amygdala)
Are bone fractures remodeled or repaired?
Repaired
Name the steps of bone repair
1) Inflammation/ Hematoma formation (within hours of fracture or surgery; day 1-5)
2) Procallus formation by osteoblasts (within days)
3) Fibrocartilaginous callus formation (day 5-11)
4) Bony callus formation (day 11- 28)
5) bone remodeling (day 18 onwards, lasts months to years)
Describe what happens in the hematoma formation stage of bone repair
- Immediately follows fracture
- Blood vessels to bone/ periosteum are rupture, causing hematoma around fracture site.
- Hematoma clots, forms temporary frame for healing
- Injury to bone results in secretion of pro inflammatory cytokines
- Osteoclasts and other cells (macrophages, lymphocytes) act together to remove damaged bone and issue and release factors to stimulate healing
Describe what happens in the fibrocartilaginous callus formation stage of bone repair
- Growth factor leads to angiogenesis, granulation tissue begins to develop
- Osteocytes differentiate into fibroblasts, chondroblasts, and osteoblasts
- Collagen rich fibrocartilage network develops to span fracture ends; has hyaline cartilage sleeve
- Layer of woven bone laid done
Describe what happens in the bony callus formation stage of bone repair
- Cartilagenous callus begins to undergo ossification
- RANK L is expressed, stimulating further differentiation of chondroblasts, chondroclasts, osteoblasts, and osteoclasts. Cartilage resorbed and beings to calcify
- Woven bone layed down
- Results in hard, calcified callus of immature bone
Describe what happens in the bone remodelling stage of bone repair
- Continued migration of osteoblasts and clasts- repeated remodelling
- Resorption by osteoclasts, new bone formation by osteoclasts
What is the main function of osteoblasts
osteoBlasts BUILD (bone remodelling)
What is the main function of osteoclasts
osteoClasts COLLAPSE (bone resorption)
What is the significant of RANK- L in bone repair
- produced in response to bone damage; regulates osteoclast formation and activation in bone remodeling
What is the significance of osteoprotegerin (OPG) in bone repair
-produced by osteoblasts; binds to RANK L so it cannot act at receptor, which protects bone from excessive resorption
What is the region behind the knee called? What does it contain?
Popliteal fossa; contains popliteal vessels and the tibial and common fibular nerves. It is the transition between the thigh and the leg
What does the tibial nerve innercate
Posterior compartment of leg muscles
What does the deep fibular nerve innervate
Anterior compartment of leg muscles
What does the superficial fibular nerve innervate
Lateral compartment of the leg
What is the major tendon of the lower leg, and what is its function?
Calcaneal tendon (Achilles tendon)
Walking, running
What does the gastrocnemius tendon connect?
Gastrocnemius muscle to calcaneal tendon
What is the action of the gastrocnemius
Plantarflexes (toes to the floor) foot at the ankle and flexes leg at the knee joint
Action of soleus
Plantarflexes foot at the ankle, steadies’ leg over the foot
Action of plantaris
Weakly assists Gastrocnemius
Plantaris tendon connects to the ankle, close to the calcaneal tendon
Action of popliteus
Weakly flexes leg at knee and unlocks it (rotates femur on the fixed tibia)
Action of flexor hallucis longus and flexor digitorum longus
Flexor hallucis longus Flexes (curls down) great toes at all joints and plantarflexes foot at the ankle
Flexor digitorum longus Flexes lateral four digits and plantarflexes foot at the ankle, supports longitudinal arches of foot
Action of tibialis posterior
Plantarflexes foot at ankle and inverts foot (tip foot up so the sole of the foot faces the medial aspect of the person)
Tibialis posterior tendon connects this muscle to the ankle
What are the muscles of the anterior compartment of lower leg? Describe their function
Tibialis Anterior Dorsiflexion/inversion of foot
Extensor hallucis longus Extends (straighten) great toes and dorsiflexes foot at the ankle
Extensor digitorum longus Extension of lateral four digits and dorsiflexes foot
Forms 4 tendons superior to the foot and enters the dorsum of the foot along with the tendon associated with the fibularis tertius > splits in to 4, each inserting onto a toe
Fibularis tertius (arises from inferior portion EDL – not present in all individuals) Dorsiflexes foot/Extension of great toe
What is the primary function of the posterior compartment of lower leg
flex ankles and toes
What is the primary function of the anterior compartment of lower leg
extensors (dorsiflexion) of foot at ankles and toes
What are the muscles of the lateral compartment of lower leg? What is their primary function?
Primary function is to evert the foot, and weakly plantarflex foot at ankle
Fibularis Longus Everts foot and weakly plantarflexes foot at the ankle
Fibularis Brevis Everts foot and weakly plantarflexes foot at the ankle
Name the three tendons of the foot/ ankle
- Plantarflexor tendons
- Dorsiflexor tendons
- Fibularis tendons
What are the two muscles on the top of the foot? What do they do?
extensor digitorium and hallucis brevis; extend the toes
How many layers of muscle are in the bottom of the foot? What are they innervated by
four
Medial or lateral plantar nerves (comes from the tibial nerve)
Name the 3 muscles of the first layer of sole of foot
Abductor Hallucis Abducts (moves away from midline) and flexes the great toe
Flexor Digitorum Brevis Flexes lateral four digits
Abductor digiti minimi Abducts and flexes the little toe
Name the muscles (5) of the second and third later of the sole of foot
Quadratus Plantae (2nd) Assist flexor digitorum longus in flexing lateral four digits
Lumbricals (2nd) Flex metatarsophalangeal joints and extend interphalangeal joints of lateral four digits
Flexor Hallucis Brevis (3rd) Flexes proximal phalanx of big toe
Adductor hallucis (3rd) Adducts (towards midline) big toes, assists in maintaining the transverse arch of the foot
Flexor digiti minimi brevis (3rd) Flexes proximal phalanx of little toe, thereby assisting with its flexion.
Name the muscles (2) of the fourth layer of the sole of the foot.
Planta interossei (three muscles) Adducts digits 3-5, flex metatarsophalangeal joints, extend phalanges
Dorsal interossei (four muscles) Abduct digits 2-4, flex metatarsophalangeal joints and extend phalanges
Describe the knee joint
Large hinge
Synovial
Allows for flexion/ extension of lower limb
What are the main articular areas of the knee?
femorotibial
femoropatellar
What does the stability of the knee joint rely on?
Tibiofemoral ligaments
Quadricepts
Function of ACL
Prevents posterior slipping of femur on tibia; torn in hyperextension, and prevents hyperextension of knee
Function of PCL
Prevents anterior slipping of femur on tibia, shorter and stronger than ACL. Prevents posterior translation of tibia, and hyperflexion of knee
Function of MCL
Limits extension and abduction of leg, attached to medial meniscus
Function of LCL
Limits extension and adduction of leg, overlies popliteus tendon
Describe the meniscus of the knee
Made of fibrocartilage, and has thick external margins with unattached edges, that allows for joint congruency, load distribution and joint stability
What are common mechanisms of injury of the knee
Sharp turns when knee is twisted, while the foot is firmly on the ground
Compressional, rotational, shear stress on meniscus could cause a meniscal tear
twisting knee after planting foot is a common mechanism for ACL injuries, which could be complicated by a Segond fracture (avulsion fracture of lateral aspect of tibial plateau)
Lateral force applied to the knee with the foot on the ground
Common S&S of injury of knee (sprain or meniscal tear)
Popping noise may be heard
Tearing sensation with acute pain may be felt
Pain, swelling, clicking/crepitus with walking/knee extension
Inability to fully extend/lock knee (more commonly in anterior meniscus tears)
Post ACL injuries— knee may “give out” when walking/standing
What test is indicative of ACL rupture?
Lachman test
Patient lays supine, then bends affected knee 20-30 degrees, provider grasps limb over distal femur and proximal tibia, then pull forward and push backward. If there is movement 5mm or more than in normal limb, indicative of ruptured ACL
What is the anterior drawer test
Used to dx ACL injury
Patient is supine on table with hip flexed 45 degrees, knee at 90 degrees, examiner sits on patient’s foot to stabilize it, place hands on upper calf and firmly pulls tibia forward. A movement of. 5mm or more is positive
Test normal limb first and compare result with normal limb
What is the most common knee injury?
MCL sprain - usually sports related, from outside blow to knee or rapid change in direction/ speed
What test is used to dx PCL injury?
Posterior drawer test
With the knee flexed to 90 degrees and the foot stabilized (often the examiner sits on the patient’s foot), the proximal tibia is grasped firmly with both hands and the tibia is forcibly pushed posteriorly, noting any laxity compared with the other side.
What test is used to confirm MCL sprain
valgus (or abduction) stress test with the knee in both 30 degrees and 0 degrees of flexion looking for joint laxity
Describe the mechanism of injury for knee meniscal tears
Acute (most often from twisting injuries when foot remains planted) and CHRONIC (degenerative tears in older patients that can occur with minimal twisting or stress)
Signs and symptoms of knee meniscal tear
-degree of pain at time of injury = variable à followed by insidious onset of pain and swelling over 24h
-pain is exacerbated by twisting/pivoting movements
-some patients may describe a “tearing” or “popping” sensation at the time of injury
-patients can present weeks after injury and often c/o popping, locking, catching and the knee “giving out” or may just report that the knee is not moving properly
-feeling of instability is r/t a meniscal fragment floating between 2 articular surfaces à sensation that the nee is not in the position it should be
-locking = inability to fully extend knee d/t interference of torn meniscus
-effusions are common (particularly w/ large or complex tears) and can occur intermittently from tears assoc with degen arthritis (Pts with effusion typically complain of stiffness, rather than swelling)
What is chondromalacia?
-softening, inflammation, degeneration/ erosion of hyaline cartilage at a joint (affects articular cartilage surfaces of bone)
How does destruction of cartilage occur in chondromalacia?
Destruction/ degeneration of cartilage can occur from:
Cytokines/ proteolytic enzymes (i.e., resulting from intra-articular infection)
Chondrotoxic substances (i.e., from iatrogenic injections)
Microtrauma from repeated activities (due to compressive stress on joint)
Aging (decreased number of chondrocytes, therefore decreased proteoglycans, reducing water content of cartilage)
What is the most common kind of chondromalacia?
Chondromalacia patella
Describe S&S, Dx of chondromalacia patella
S&S: Anterior knee pain that worsens with stress on patellofemoral joint (climbing stairs, squatting, running)
Dull, aching
Usually does not cause swelling
Dx History (evaluate risk factors), physical evaluation
Clark’s test (evaluates patellofemoral grinding and pain by compressing patella into femoral trochlea, and having pt contract quads to pull patella through groove)
XR to rule out ddx
MRI can help in diagnosis/ staging
What is the patho of de quervain tenosynovitis
- Affects the abductor pollcis longus (APL) and the extensor pollcis brevis (EPB) tendons.
Two of the main tendons to the thumb that assist with bringing the thumb out away from the index finger (APL) and straightening the joints of the thumb (EPB).
These two tendons arise from muscles in the forearm and then run together in a sheath that keeps them close to the bone as they cross over from the thumb side of the wrist into the hand.
Any swelling of the tendons (De Quervain’s ) and/or thickening of the sheath can result in a situation where the tendons no longer fit well inside the sheath. This results in increased friction and pain with certain thumb and wrist movements.
This condition can cause pain and tenderness along the thumb side of the wrist.
S&S de quervain tenosynovitis
-radial side wrist pain
-worsened by wrist and thumb movement, radial and ulnar deviation of the wrist
-difficulty with tasks like opening jar lid, moving thumb, forming fist, grasping something, turning wrist, lifting child
-tenderness over the radial styloid
-fusiform (sausage shaped) swelling in this region
What is the finkelstein test?
test for de quervain tenosynovitis
- Thumb flexed and held inside fist
- Patient actively deviates the wrist
- Causes sharp pain along the radial wrist at first dorsal compartment
tx de quervain tenosynovitis
-can be self limited and may resolve without intervention
-persistent symptoms: splinting, anti-inflammatories, corticosteroid injection
-operative management if symptoms fail to improve/ recur after 2 corticosteroid injections (release tendon sheath to make more room for irritated tendons)
Describe pathophysiology of rheumatoid arthritis
-Chronic systemic autoimmune disease that primarily involves the joints.
-Prominent immunologic abnormalities include immune complexes produced by synovial lining cells and in inflamed blood vessels.
-Released inflammatory mediators and various enzymes contribute to the systemic and joint manifestations of rheumatoid arthritis (RA), including cartilage and bone destruction.
-Rheumatoid nodules develop in about 30% of patients with RA. They are granulomas consisting of a central necrotic area surrounded by palisaded histiocytic macrophages, all enveloped by lymphocytes, plasma cells, and fibroblasts
Describe common characteristics RA
-affects same joints on both sides of body (symmetrical arthritis)
-starts at small joints and moves on the larger joints as disease progresses
-fingers may be bent (boutonniere or swan neck deformities)
-tendons on hand may be prominent (bowstring sign)
-stiffness, pain, redness, warmth to touch, swelling
-joint stiffness worse in the morning and after being still; persists >1h
-can have extra articular sx (vasculitis, effusions, pericarditis, subcut RA nodules…)
Dx RA
*Differentiate Inflammatory from Non-inflammatory Arthritis
*Differentiate RA from Other Inflammatory Arthritides
*RA is a clinical diagnosis. Referral to a specialist should not be based on the results of lab tests if there are no clinical features suggesting RA. There are no tests that can reliably make the diagnosis of RA.
- If there are clinical features then the following lab tests may be useful for monitoring and ruling out other types of arthritis: CRP, ESR, RF, ANA, X-rays, joint aspiration.
*CRP is preferred test (covered by MSP).
Tx RA
*Urgent management is important because early recognition and intervention has been shown to improve outcome.
*Disease modifying anti-rheumatic drugs (DMARDs), particularly when used early, change the course of the disease and are proven to reduce damage and associated disability.
*Aim is to not only treat symptoms, but to also treat the disease progression to prevent permanent joint damage.
*Treatment is multi-disciplinary
*NSAID and acetaminophen for pain management
* severe symp can add prednisone
*follow up q 3-6 months
Pathophysiology osteoarthritis
-OA sometimes begins with tissue damage from mechanical injury (eg, torn meniscus), transmission of inflammatory mediators from the synovium into cartilage, or defects in cartilage metabolism.
-Obesity triggers some of these defects in cartilage metabolism, leading to cartilage matrix damage and subchondral bone remodeling mediated by adipokines such as leptin and adipsin. The tissue damage stimulates chondrocytes to attempt repair, which increases production of proteoglycans and collagen. However, efforts at repair also stimulate the enzymes that degrade cartilage, as well as inflammatory cytokines, which are normally present in small amounts.
-Inflammatory mediators trigger an inflammatory cycle that further stimulates the chondrocytes and synovial lining cells, eventually breaking down the cartilage. Chondrocytes undergo programmed cell death (apoptosis). Once cartilage is destroyed, exposed bone becomes eburnated and sclerotic.
What does secondary OA result from
conditions that change microenvironment of cartilage (trauma, metabolic defects, infections, endocrine and neuropathic disorders, RA, etc)
What is the most common joint disorder
Osteoarthritis
T/ F OA is nearly universal by age 80
True. May not be symptomatic- only half patients with pathologic changes of OA have symptoms
Earliest symptom of OA?
Pain- deep ache. Usually worse with weight bearing and relieved by rest. Stiffness following awakening/ inactivity, but lasts <30 min and lessens with movt
What causes joint enlargement that is characteristic of OA?
As OA progresses, joint motion becomes restricted, and tenderness and crepitus or grating sensations develop. Proliferation of cartilage, bone, ligament, tendon, capsules, and synovium, along with varying amounts of joint effusion, ultimately cause the joint enlargement characteristic of OA.
t/f acute synovitis is common in OA
F- usually chronic processes
How to dx OA
-xr of symptomatic joints
-labs usually normal, but used to rule out other disorders
-if causing joint effusions, synovial fluid analysis can help differentiate it from inflammatory arthritises (OA= clear, viscous, WBC < 2000)
Tx goals OA
Treatment goals are relieving pain, maintaining joint flexibility, and optimizing joint and overall function.
