Flashcards in Midterm 3: Buzzword Bingo Deck (479):
Types of bones that use endochondral bone formation
Long bones (humerus, femur, metacarpals, etc); short bones (carpals, tarsals, etc)
Cartilage model of bone forms -> starts to ossify from center outward
Endochondral bone formation
Types of bones that use intramembranous bone formation
Flat bones - clavicle, scapula, bones of the skull, bones of the pelvis
Embryonic mesenchymal cells cluster, differentiate into osteoblasts -> osteoblasts form spicules of bone that coalesce into bone plates
Intramembranous bone formation
Defect in this process leads to underdeveloped or absent clavicles, dental anomalies, larger fontanelles at birth, and osteoporosis
Intramembranous bone formation -> the disorder described is clavicocranial dysplasia
Autosomal dominant mutation in Cbfa1/Runx2
Claviocranial dysplasia - these are transcription factors in genes needed for osteoblast differentiation, so the mutation has the biggest effect on intramembranous bone formation
Impaired cartilage differentiation and growth may impact what kinds of bone development?
Endochondral bone formation, so long and short bones, but not so much flat bones
Zone of the epiphyseal plate that is the most common site of fracture
AD (heterozygous) mutation leading to constitutive activation of FGFR3 at the proliferative zone of bone
Slows proliferation of bone -> achondroplasia
Part of bone responsible for increasing in length
Dense bone in diaphysis that transmits force efficiently
Type of bone found in metaphysis/epiphysis that provides cushioning
The triangular piece of bone that breaks off when a bone is broken under an axial load that is too strong. The side under tension cracks in a direction perpendicular to the axial load, but the side under compression shears, producing the triangular "butterfly fragment"
Cell that controls signaling for bone remodeling, mineralizes bone, and produces type 1 collagen
Long-lived cell embedded in bone that maintains calcium homeostasis and plays a role in mechanotransduction within the bone
Cell of hematopoietic origin that looks like a multinucleated giant cell and releases carbonic anhydrase to break down bone
Bone cells of mesenchymal origin
Osteoblast -> osteocyte
Bone cells of hematopoietic origin
Functional unit of cortical bone
A receptor on osteoclasts that activates signaling pathways to result in bone resorption
A molecule secreted by osteoblasts that can activate osteoclasts
Cellular target of action of activated vitamin D/PTH (what they act on)
Osteoblasts -> induce release of RANKL
Consequence of continuous over-secretion of PTH
"Brown tumors" - a vascular, fibrous lesion that occurs when hyperparathyroidism causes too much bone resorption in order to release more calcium
Net action of pulses of PTH or synthetic analogue (teriparatide)
Drug class that mimics the structure of inorganic phosphate and leads to osteoclast apoptosis
Tumor releases lots of RANKL -> what happens?
RANKL >> OPG, so there is too much bone resorption -> lytic lesions. Occurs in giant cell tumors, multiple myeloma, metastatic breast cancer
Tumor releases lots of OPG -> what happens?
OPG >> RANKL, so there is too much bone formation -> blastic lesions. Occurs in prostate cancer
Molecule that binds to RANKL and prevents osteoclast activation
OPG knockout mouse would have bones that looked like...
Osteoporotic bones! Very low bone density, since OPG induces bone formation by inhibiting bone resorption.
RANKL or RANK knockout mouse would have bones that looked like...
Hyperdense bones! Not enough RANKL/RANK action would lead to a lack of bone resorption, leading to very dense but probably structurally problematic bones.
RANKL Ab that essentially acts like synthetic OPG, preventing RANK/RANKL interactions and inhibiting bone resorption
Osteoblasts are responsible for signaling for which aspects of bone remodeling?
Formation and resorption
RDA for calcium
1000 mg/day for most adults, more for adolescents, pregnant/lactating women, post-menopause, men over 70
Main goal of PTH secretion
Raise calcium levels
Blood Ca++ is low -> what does parathyroid do?
Blood Ca++ is high -> what does parathyroid do?
Prevent secretion of PTH
If the calcium sensing receptor in the kidney senses high Ca++, what does the kidney do?
Excrete calcium in urine
If the calcium receptor in the kidney senses low Ca++, what does the kidney do?
Reduce excretion of calcium in urine
MOA of PTH at kidney
Increase Ca++ resorption, inhibit phosphate resorption (because phosphate binds Ca++ and lowers available calcium), increases activation of vitamin D by 1-a-hydroxylase because that increases gut absorption of Ca++
MOA of PTH at bone
Bind to receptors on osteoblasts -> activate osteoclasts -> increased bone turnover -> release of calcium and phosphate into blood
High PTH leads to increased secretion of what signaling molecule by osteoblasts?
If blood Ca++ is high, what should PTH levels be?
If levels of 1,25-D are high, what should PTH levels be?
How do Ca++ and phosphate levels change in response to 1,25-D?
1,25-D leads to both increased Ca++ (in conjunction with PTH) and increased phosphate
MOA of 1,25-D at GI tract
Stimulate Ca++ and phosphate absorption
MOA of 1,25-D at parathyroid gland
Decrease PTH production and cell proliferation there
MOA of 1,25-D at bone
Maintenance of adequate minerality of bone
Best marker to measure vitamin D status
25-D -> the formation of this is unregulated so this reflects total vitamin D entering the system
Step of vitamin D activation that is most highly regulated
Activity of 1-a-hydroxylase
Effect of PTH on 1-a-hydroxylase
Induces its activity in order to raise Ca++ levels by creating more 1,25-D
Inducers of 1-a-hydroxylase activity
PTH, low phosphate
Inhibitors of 1-a-hydroxylase activity
High Ca++, 1,25-D
This protein is structurally similar to PTH, shares a receptor, and if its levels are abnormally high (like in some cancers), it can mimic excess PTH
Does human calcitonin have an appreciable effect on bone and calcium, as far as we know?
Cells that produce calcitonin
C-cells of the thyroid
Key biomarker for determining etiology of hypercalcemia or hypocalcemia
PTH levels - will determine if this is a parathyroid problem or due to an external factor
High Ca++, low/normal phosphate, decreased bone density, high or inappropriately normal PTH. Urinary calcium low
Primary hyperparathyroidism - bones, stones, groans, and psychiatric overtones
Patient with brown tumors, abdominal pain, kidney stones, and confusion
Uncontrolled primary hyperparathyroidism
Treatment for primary hyperparathyroidism
Surgical removal of affected gland - usually curative
Patient with a failed parathyroidectomy - what might you suspect?
Familial hypocalciuric hypercalcemia - rare AD disorder due to a LOF mutation of calcium-sensing receptors
Patient with malignancy (not of the parathyroid gland) and hypercalcemia - what could be causing the hypercalcemia?
Invasion/destruction of bone by tumor, production of PTHrP by tumor, production of vitamin D by the tumor
Patient with a granulomatous disease like TB or sarcoidosis and hypercalcemia - why?
Unregulated 1a-hydroxylase activity
Hypercalcemia, renal failure, and metabolic alkalosis
Hypercalcemia in a patient who has been immobilized in the ICU - why?
Demineralization and increased bone resorption due to prolonged immobilization
Low calcium, low or inappropriately normal PTH
Primary hypoparathyroidism, found in DiGeorge syndrome (22q11 deletion), post-surgical, or autoimmune
Low or normal calcium with high PTH
This is normal - this is why we have parathyroid glands. Called secondary hypoparathyroidism, though.
Common causes of secondary hypoparathyroidism
Vitamin D deficiency, renal failure
Effect of compressive force on bone
Bone growth (electronegative force)
Effect of tensile force on bone
Bone resorption (electropositive force)
Potential for healing in a kid with an injury to bone but not growth plate
Good! Can heal almost completely because an intact growth plate tends to straighten itself out over time
Treatment for an injury involving growth plate
Recognize, reduce the fracture gently but accurately, adequate fixation (don't fixate the physis if possible), monitor for late growth disturbance
Bone response to low load
Loss of bone mass via resorption
Bone response to a gradual increase in load above physiologic load
Increased bone mass
Repetitive microdamage to bone
Acute overload of bone
A bone healing that starts with inflammation and a hematoma, followed by formation of a soft callus made of osteoid that surrounds the hematoma, followed by a hard callus forming as fiber bone replaces the osteoid, followed by corticoremodeling
Secondary bone healing
Bone healing after internal fixation, where cutting cones are formed by osteoblasts going in both directions to cross the break and heal the cortex
Primary bone healing
Older patient with progressive vision loss seen over time, and straight lines do not appear straight in their vision
Macular degeneration - blood in the antral vision/degeneration there. The phenomenon known as metamorphopsia is seeing straight lines as curved. This is urgent but not emergent.
Dark visual loss with flashes, followed by floaters, followed by a "curtain"
Retinal detachment - flashes are tugging of the retina due to fluid from a tear in the retina, floaters are RBCs getting behind the retina, and the curtain is retinal detachment
If 50% or more of the retina is detached, what sign is visible?
Rapid afferent pupillary defect
"Smoky" vision in a diabetic
Causes of vitreous hemorrhage
Proliferative diabetic retinopathy, retinal tear, valsalva maneuver, trauma
Urgent or emergent: Macular degeneration
Urgent - same day ophtho
Urgent or emergent: retinal detachment
Urgent - same day ophtho
Urgent or emergent: vitreous hemorrhage
Urgent - same day ophtho
Pale or white retina with a cherry red spot and RAPD, profound visual loss
Central retinal artery occlusion
Urgent or emergent: central retinal artery occlusion
EMERGENT! Do ocular massage to get the embolus out and page ophtho ASAP
History of hypertension; retinal exam shows "blood and thunder" (torturous vessels and multiple areas of blood in retina)
Central retinal vein occlusion
Urgent or emergent: central retinal vein occclusion
Not as urgent - next day ophtho
Cause of central retinal vein occlusion
vein gets compressed by central retinal ophtho
Important management of central retinal vein occlusion, besides sending to ophtho next day
Treat hypertension to prevent this occurring in the other eye!
Corneal edema, deep eye pain, sudden decrease in vision, nausea, vomiting, halos in vision, eye is hard to the touch, pupils fixed and mid-dilated
Angle closure glaucoma
Urgent or emergent: angle closure glaucoma
EMERGENT! Call ophtho right away
Relative afferent pupillary defect, eye pain that is worse with movement, central scotoma, and decreased color vision
Pathophysiology of angle closure glaucoma
The angle of the anterior chamber gets clogged - this can occur with dilation of the pupils, especially if someone has a positive volcano sign
Pathophysiology of optic neuritis
Swollen optic nerve in 1/3 of patients, but the symptoms are caused by optic nerve inflammation leading to demyelination. This is a common early manifestation of multiple sclerosis.
MRI findings in optic neuritis
periventricular white matter lesion
Urgent or emergent: optic neuritis
Can refer next day - not all that urgent
Moderate to severe vision loss, relative afferent pupillary defect, decreased color vision, altitudinal visual field issues
Ischemic optic neuropathy
Urgent or emergent: ischemic optic neuropathy
Urgent - same day referral
Patient with ischemic optic neuropathy and scalp tenderness or jaw claudication: workup
Suspect giant cell arteritis - this makes it a more urgent situation. Start steroids right away, get labs (ESR, CRP), order temporal artery biopsy
Patient with headache, homonymous hemianopia
Occipital lobe stroke
Urgent or emergent: occipital lobe stroke
Medical emergency!! Call the stroke team
Patient with occipital lobe stroke: results of important CN II tests
Visual acuity may be 20/20... that's because it's not the optic nerve that's affected! Important thing to check is visual fields, to look for deficits in one half of the visual field (homonymous hemianopia)
Patient complaining of dark vision lasting for 5-10 minutes, then resolving spontaneously
Transient monocular visual loss (amaurosis fugax)
Pathophysiology of transient monocular visual loss
Small embolism in retinal vessels causes transient ischemia, leading to visual loss. It is spontaneously broken down, which is why you get the return of vision after 5-10 minutes.
Important management for transient monocular visual loss
Workup for thromboembolic events, clots, friable plaques, heart issues, giant cell arteritis
Urgent or emergent: transient monocular visual loss
Usually work up emergently if it occurred within the past few days, to check for underlying causes (do a carotid doppler, echo, labs, etc)
Type of cartilage on articular surfaces, the ribs, nasal septum
Type of cartilage on auricle of ear, trachea, auditory tube
Type of cartilage at tendon/ligament junction with bone, annulus fibrosus of intervertebral disc, menisci
Developmental origin of cartilage in the head
cranial neural crest
Developmental origin of cartilage in the limbs
lateral plate mesoderm
Developmental origin of cartilage in the axial skeleton
Biggest molecular component of cartilage (and the other components)
Main component is water, followed by collagen, then proteoglycan, then non-collagenous protein, then cells
Major component of extracellular matrix dry weight
Component of cartilage that provides its framework and tensile strength
Component of cartilage that provides its compressive strength and attracts water
Function of anchorin CII
anchors chondrocytes to collagen
Function of cartilage oligomeric matrix protein
maintain properties and integrity of collagen network
Function of fibronectin in cartilage
Matrix organization and stability
Function of tenascin in cartilage
Cell adhesion and cell-matrix interactions
How are nutrients transported through cartilage to chondrocytes?
Cartilage is avascular so nutrients are transported via diffusion in the massive amount of water that contributes to cartilage.
Describe the structure of proteoglycan
Chondroitin sulfate molecules link onto the core protein, forming a proteoglycan. These then aggregate as attachments on hyaluronic acid through a link protein.
Composition of elastic cartilage
Collagen type II and elastic fibers
Composition of hyaline cartilage
mostly collagen type II and aggrecan (proteoglycan), some type I collagen
Composition of fibrocartilage
Type I and II collagen, basically combined hyaline cartilage with dense connective tissue
Which types of cartilage have a perichondrium, and what is it?
Hyaline and elastic cartilage have a perichondrium, which is a fibrous outer layer with fibroblasts that is on top of a chondrogenic region with stem cells.
Cartilage that forms in the healing response to injury
Cartilage that bests tolerates repetitive deformation
Cartilage that is strongest and best for mechanical support
Role of hyaline cartilage in joints
Reduce friction and distribute loads
4 zones of articular hyaline cartilage
Superficial zone, middle zone, deep zone, calcified zone. The middle zone is the thickest.
Zone of articular cartilage with smaller, flatter cells secreting lubricin
Superficial or tangential zone
Orientation of collagen II fibers in superficial zone
parallel to surface (same orientation as the flattened chondrocytes)
Zone of articular cartilage with rounded/oval, bigger, metabolically active cells making collagen
Organization of collagen fibers in middle zone
Zone of articular cartilage with spherical chondrocytes arranged in columns, the most proteoglycan of any layer, and the least water
Orientation of collagen fibers in deep zone
perpendicular to surface (vertical)
Zone of articular cartilage characterized by hypertrophic chondrocytes expressing collagen X and MMPs to degrade the ECM
Line separating cartilage from subchondral zone
Why is collagen X important?
It is a precursor to bone formation
Why does the calcified zone produce MMPs?
To degrade ECM and allow for bone formation
A constant load on cartilage produces a time-dependent deformation - what is this called?
A constant deformation of cartilage results in time-dependent stress: what is this called?
Growth factors important for chondrogenesis
FGF, TGFbeta, BMP, WNT
Chondrocytes divide in lacunae of cartilage into chondroblasts, which mature into chondrocytes, leading to increasing cartilage diameter
Interstitial cartilage growth - embryonic process
At the edges of the cartilage, stem cells divide into chondroblasts and then into chondrocytes in the perichondrium, leading to increased length
Appositional cartilage growth
Changes in collagen with aging
Fewer but bigger chondrocytes, less water, more collagen crosslinking, less proteoglycan -> increased stiffness, more glycosylation end products
Favored type of metabolism for chondrocytes
First step in hip osteoarthritis management
Conservative, non-operative management - PT, weight reduction, anti-inflammation. Surgery is normally elective
Joint-sparing hip osteoarthritis surgery
Osteotomy, core decompression, or hip arthroscopy
Major limitations of total hip arthroplasty
Obesity, comorbidities (BMI>40 is a huge contraindication). Also poses a risk of osteolysis/bone loss
RFs for hip fracture
F>M, smoking, EtOH, decreased VitD, thin, caucasian, post-menopausal
Repair for an intertrochanteric hip fracture
Can be fixed via plates or screws depending on the fracture itself
Repair for a femoral neck fracture
Since it damages blood supply to the femoral head, a partial or total hip replacement is needed.
Morbidity for a hip fracture
High - around 20% within one year since many of these patients are sick or fragile to begin with
Groin pain, restricted and painful hip ROM especially on internal rotation, Trendelenberg test, loss of joint space on XR
Back, hip, or vascular? Groin pain
Back, hip, or vascular? Low back or buttock pain
Back, hip, or vascular? Calf pain on exercise
Vascular (although need to rule out neurogenic claudication as well)
Back, hip, or vascular? Not a lot of radiation of pain, if it's present it only goes to the knee
Most likely hip, which doesn't tend to have a lot of radiating pain
Back, hip, or vascular? Pain radiates down below the knee following a dermatome
Back - radiculopathy
Back, hip, or vascular? Patient has a limp and has trouble tying shoes
Back, hip, or vascular? Pain is better with back flexion
Back, hip, or vascular? Pain follows a particular pattern, occurs at a specific distance of walking, and gets better with rest
Back, hip, or vascular? Decreased hip ROM that reproduces pain
Back, hip, or vascular? Positive straight leg test and neuro findings
Back, hip, or vascular? Loss of leg hair
If you suspect that leg pain is due to a vascular cause, what should you do as a test?
Prevention of hip fracture
Maintain bone health with calcium, vitamin D, osteoporosis drugs as needed. Fall prevention as well
Goals for obese patients prior to elective hip or knee replacement
Lose weight (BMI below 40 ideally), metabolic control, optimize nutrition
First imaging step for hip pain
Plain films - you don't need MRI right away to see osteoarthritis
Function of the menisci of the knee
What's a risk of meniscectomy that explains why it's not really done any more?
Taking out the meniscus leads to increased loads on the joint and an increased risk of osteoarthritis at the knee
Causes of knee DJD
Obesity, genetics, old trauma, loss of meniscus, chronic instability, malalignment
Imaging for diagnosis of meniscal tears
MRI, in addition to exam
Pain at the knee joint line
Repair of meniscal tears
Repair via arthroscopy/joint preservation, observation, or (less commonly) meniscectomy)
Initial treatment of knee osteoarthritis
Decrease loads: weight loss, activity modifications, and unloader braces
PT: try to improve strength and ROM
Purpose of a tibial osteotomy
Correct a bow-legged deformity
Foreign body sensation in eye, swollen eyelids, itching, crusting
Blepharitis - inflammation of melbomian glands
Tx for blepharitis
Lid hygiene with diluted baby shampoo, ABX or steroids, lubricants. If it presents with rosacea in a severe form, treat with doxycycline
Staph infection of a melbomian gland causing cellulitis
Tx for chalazion
hot compresses, massage, topical ABX and steroids, I&D
Red, indurated, painful eyelid without proptosis or blurred vision
Preseptal cellulitis - caused by trauma, sinus infection, eyelid margin infection
Tx for preseptal cellulitis
oral ABX and monitor for orbital cellulitis
Red, indurated, painful eyelid with diplopia, vision loss/RAPD, and/or no improvement with oral ABX
Diagnostic test for orbital cellulitis
Tx for orbital cellulitis
IV ABX and surgical drainage
Vesicles on unilateral face with involvement of the tip of the nose (pain to palpation)
Shingles of V1 nerve root with Hutchinson's sign
Tx of shingles
Nasolacrimal duct infection
Test for corneal pathology
Fluorescein dye - dab it on the anterior fornix and visualize with cobalt blue. It stains corneal epithelium
In regard to eye pathology: define injection
Torn area of corneal epithelium, painful, stains with fluorescein
Tx for corneal abrasion
topical ABX, patching, dilating drops
Pain and blurry vision with punctate staining of cornea with fluorescein
Dry eye, exposures, or contact lens overuse
Fluorescein staining with a linear branching pattern, corneal swelling leading to clouding of cornea
HSV keratitis (could also be caused by VZV but that would have a rash)
Most common cause of infectious corneal blindness
Centrally located punctate staining
Contact lens keratitis - could be viral, bacterial, chemical, amoebic, parasitic
Tx for contact lens keratitis
Discontinue use of contacts, use ABX, don't sleep with contacts
Tx for HSV keratitis
Corneal ulcer: causes and management
This is an emergency! Due to pseudomonas infection, anterior chamber infection. Get ophtho consult asap
Consider that this might be a vision-threatening cause of vision loss if you have the following symptoms:
S = sudden visual loss
T = trauma (ruptured eyeball?)
O = other signs/symptoms of scary conditions
P = pain
Red eye with sudden visual loss: DDx
corneal ulcer, cellulitis, angle closure glaucoma
Management of open globe injury
This is an emergency! Need a shield on the eye
Management of corneal foreign body
CT or XR to spot the metal, since this is most often from metal flying during activities that involve metal on metal
Blunt injury filling the eye with blood
Hyphema - this is an urgent condition
Nausea, vomiting, red eye
Angle closure glaucoma
Diplopia and red eye
Photophobia and red eye with tiny white dots on inside of cornea
Sleeps in contacts, has a red and painful eye
Worry about corneal ulcer
Deep boring pain and red eye: DDx
Angle closure glaucoma, cellulitis, iritis, scleritis
White of eye appears red
Pathophys causes of scleritis
Dilation of vessels due to inflammation or increased flow; abnormal vessels; blood outside vessels
Edema of conjunctiva
Watery or clear eye discharge
Viral etiology or dry eye, viral will often present with palpable preauricular LNs, if viral is very contagious
Purulent eye discharge
Bacterial infection - staph, strep, haemophilus. Treat with ABX
Mucoid, white-yellow eye discharge
Allergic, Tx with topical antihistamines. Often itchy!
Benign causes of subconjunctival hemorrhage
cough, sneeze, meds
360 degrees of subconjunctival hemorhage
Globe rupture - protect eye. This is emergent! Really bad if associated with an abnormal pupil
Abnormal wing of tissue in an area of eye exposed to UV, and red
Pterygium - often recurs
Superficial and mild pain and red sclera that blanches with 2.5% phenylephrine
Episcleritis - caused by dilation of vessels in the vascular plexus between the conjunctiva and the sclera. Can be idiopathic
Red sclera with a violaceous hue, with severe boring pain, often associated with autoimmune systemic disease, doesn't blanch with phenylephrine
Scleritis - this can be vision-threatening. Need ophtho consult to prevent vision loss. Treated with steroids and NSAIDS.
What is the function of the angle of the anterior chamber?
Drains fluid (aqueous humor) out of the anterior chamber. Usually 45 degrees
Pathophysiology of acute angle closure glaucoma
A bigger, more anteriorly positioned lens pushes the iris forward, causing a narrower angle of the anterior chamber. When the pupil dilates, the peripheral iris becomes thicker, and it closes off the angle and gets stuck to the lens, so aqueous humor backs up causing an increase in eye pressure, leading to pain, nausea, and vomiting.
Findings in acute angle closure glaucoma
Fixed mid-dilated pupil, dilated vessels, shallow anterior chamber, wrinkled cornea due to corneal edema
Anterior chamber filled at least partway with blood
Hyphema, due to blunt trauma compressing eye in AP direction, so it expands in other directions, potentially ripping the iris off its base
WBCs forming a hypopia in the eye, along with infection, decreased vision, severe pain
Endophthalmitis - often introduced during surgery
Limbal flush, small pupil, photophobic
Pathophysiology of iritis
Infection and genetic predisposition lead to an autoimmune response causing vasodilation of vessels at the limbus. Also called anterior uveitis
Fibrous connective tissue that attaches muscles to bone
Function of tendons
Move bones or other structures
Fibrous connective tissue that attaches bone to bone
Function of ligaments
Hold structures together, provide stability
Composition of tendons
Type I collagen produced by tenocytes, within a proteoglycan matrix
How is collagen organized in tendons?
In response to mechanical load
Loose connective tissue that allows longitudinal movement of tendons, binds tendon fascicles, and supports vessels and nerves as well
Loose connective tissue that allows movement within the tendon sheath
Synovial structure that reduces friction within the connective tissue surrounding the tendon
Tendon blood supply
Longitudinal vessels along the tendon unit with blood supply to enotenon and paratenon; diffuses across sheath to tendon
Innervation of tendon
No nerve fibers within tendon. Epi- and paratenon contain nociceptive nerve endings that terminate on the surface of the tendon, and Golgi tendon organs are at the musculotendinous junction to transmit stretch information
What can athletes do to improve the viscoelastic relationship of their tendons?
Composition of ligaments
Collagen and matrix produced by fibroblasts
Most common type of ligament insertion
Indirect insertion: superficial layer connects to periosteum, and bone is penetrated by Sharpey's fibers
Less common type of ligament insertion
Direct fibrocartilagenous insertion: tendons insert deep and superficial through four zones: ligament, fibrocartilage, mineralized fibrocartilage, bone
Blood supply to ligaments
Uniform microvascularity from the ligament insertions
Innervation of ligaments
Nociceptive fibers and proprioceptive fibers (these are for joint positioning sense, and are important in sprains because these take a long time to come back, so damage to these increases risk of re-injury)
Stress-strain relationship of ligaments
Non-linear: non-uniform recruitment of fibers
Pathophysiology of Achilles tendinopathy
The area is relatively hypovascular. Repetitive use causses microtrauma to the distal tendon (least vascularity), which probably leads to poor healing and inflammation.
Presentation of Achilles tendinopathy
Gradual onset, pain over distal Achilles tendon, thickening or nodularity, bursitis.
Painful/reduced active plantarflexion and passive dorsiflexion, but squeezing the gastrocnemius produces a passive plantarflex
Achilles tendinopathy. The Thompson test (squeeze the gastrocnemius) was negative (it produced passive plantarflexion) - if it didn't produce the plantarflexion that would suggest a tendon rupture
Do you need imaging for Achilles tendinopathy?
Not needed. May see Haglund's deformity on plain films, ultrasound may help confirm diagnosis, MRI may show thickening of the tendon.
MSK consideration with fluoroquinolones
Risk of tendon rupture - this is why we avoid prescribing them whenever possible
Initial management of Achilles tendinopathy
Ice, NSAIDs for one week, heel lifts in shoes, avoid aggravating activities, PT
Tx for Achilles tendinopathy with most evidence of benefit
Eccentric resistance-based PT, but it may take a long time and requires a lot of buy-in
Are injections helpful for Achilles tendinopathy?
Evidence is mixed... steroids are helpful for reactive bursitis but may increase the risk of rupture. Injectables have no long-term outcome differences vs placebo
When to do surgery for Achilles tendinopathy
If no improvement after 4-6 mo
MOA of Achilles rupture
Sudden maximal plantarflexion with the ankle already fully dorsiflexed
Will patients with Achilles rupture have previous S/Sx?
1/3 have Sx of tendinopathy but most probably have tendon degeneration before rupture
Squeeze a patient's gastrocnemius and get NO plantarflexion passively
Positive Thompson's test, indicates Achilles rupture
Imaging for achilles rupture diagnosis
US is ideal for showing the movement of the tendon in plantarflexion and dorsiflexion. MRI can also work
How to manage Achilles tendon rupture
Surgery will lower risk of re-rupture - probably will use surgery for athletes so that they can get back to peak performance.
2 main inflammatory causes of tenosynovitis
Systemic inflammation or inflammation due to overuse
Gradual onset of reduced active motion of tendons in wrist, may have trigger finger
Presentation of tenosynovitis of wrist
Tenosynovitis with acute onset, pain, redness, and decreased passive range of motion
Infectious etiology - need to recognize this
Tx for inflammatory tenosynovitis
Ice, splinting, NSAIDs, PT, corticosteroid injections to sheath
Tx for infectious tenosynovitis
ABX if identified quickly and non-suppurative, otherwise give broad-spectrum ABX and do surgical debridement
Insidious onset of symptoms: sharp pain in heel in the morning like "stepping on a rock" with tenderness at the anteromedial calcaneus and pain with passive dorsiflexion
Plantar fasciitis - overuse at the proximal portion of the plantar fascia
Relevance of a calcaneal spur on XR in a patient with plantar fasciitis?
Not really relevant - not the source of the pain
Tx for plantar fasciitis
Rest, NSAIDs, PT, orthotics or arch support, sleeping socks that dorsiflex the ankle all night
Second line: immobilization, corticosteroids
Grade 1 ligament tear
Partial tear, no laxity
Grade 2 ligament tear
Partial tear with laxity but a solid endpoint
Grade 3 ligament tear
Complete tear with laxity and no endpoint/soft endpoint
Bony avulsion on a ligament tear
This is more common in kids - the ligament is intact but the bone has a piece come off at the ligamentous attachment
Ligaments sprained in an inversion ankle injury
Anterior talofibular ligament, calcaneofibular ligament, posterior talofibular ligament - these are the ligaments on the lateral side
MOI of a high ankle sprain
Dorsiflexion and external rotation lead to the talus pushing out against the fibula, causing a high ankle sprain and/or fibular fracture
When to allow a joint injury patient to sit out of their sport but stay on the sidelines
Fracture (bony tenderness, crepitus, deformity) or instability without prior complications
When to allow a joint injury patient to immediately go back in to their game
If joint is stable, no fracture, and they can protect themselves
What produces a more severe injury: inversion or eversion?
Ottawa criteria for when to image ankle
Needs to have malleolar zone pain AND either tenderness over posterior lateral or medial malleolus OR can't bear weight at time of injury/for 4 steps in office
Ottawa criteria for imaging foot
Get foot films if there is mid-foot pain AND it is tender over the navicular or base of 5th OR the patient can't bear weight
Low-risk ankle rule in pediatric patients:
Don't need radiographs if ankle injury is not a high-risk fracture and it meets these criteria: Acute injury (<3 days), no underlying risk of pathologic fracture (Hx of OI, bone lesion, etc), no congenital ankle or foot malformation, child can express pain or tenderness, and tenderness/swelling is limited to the distal fibula or the ligaments surrounding it below the level of the anterior tibial joint line.
*Injuries which can be managed functionally with splinting and return to activity as tolerated are deemed low-risk: sprains, nondisplaced SH I and SH II, of distal fibula, avulsions of distal fibula or lateral talus
Best management of ankle sprains
RICE, walking boot or bracing, PT early and often to improve proprioception
How to help prevent ligament injuries
Neuromuscular training programs - high risk reduction
Most common direction for a GH dislocation
Anterior inferior direction
Where does the long head of the biceps tendon anchor in the shoulder?
Superior labral cartilage
Important stabilizers of the shoulder
Superior, middle, and inferior GH ligaments and the ligaments stabilizing the AC joint
Dynamic stabilizers of the shoulder
Rotator cuff muscles, especially subscapularis and its tendon in the anterior direction
MOI of a GH dislocation
Indirect force with arm abducted and externally rotated, OR direct force - blow from posterior shoulder
Patient with a prominent posterior acromion and sulcus sign (skin tight over edge of acromion), in a lot of pain, arm carried in abduction/internal rotation
GH dislocation in anterior direction
Ideal immediate management of GH dislocation
Reduce the dislocation acutely, in the ED with sedation if needed
Tx of shoulder dislocation after reduction
PT necessary because there's a high recurrence rate. Surgical stabilization is an option.
Imaging for GH dislocation
Pre-reduction and post-reduction plain films from at least two views - AP and scapular Y or axillary
Other structures that may be injured in a GH dislocation
Axillary nerve... But this usually resolves quickly.
Anterior inferior labrum - if this is injured, there is a particularly high recurrence rate.
Grade 1 AC separation
Stretched AC ligament, no deformity, normal XR
Grade 2 AC separation
Complete tear of AC ligament, may or may not have deformity or widening on XR, laxity of ligament
Grade 3 AC separation
Complete tear of AC and coracoclavicular ligaments - laxity, deformity (distal clavicle elevation), widening of joint on XR, unwilling to use arm
MOI of shoulder AC separation
Direct blow to lateral shoulder
How to manage axillary neuropraxia after GH dislocation
Watch and wait - this is common and usually resolves in a few days
Capsular contracture and inflammation leading to restricted passive ROM, nothing else appears to be wrong, normal MRI
Adhesive capsulitis aka frozen shoulder
How to diagnose adhesive capsulitis
Diagnosis of exclusion - MRI will be normal
RFs for adhesive capsulitis
F>M, ages 30-60, often bilaterally but usually spaced a few years apart, and never affects same shoulder twice. Can have an insidious onset or can occur if there is trauma w/o significant damage to shoulder joint that leads to inflammation and then stiffness. Diabetes and thyroid disease - may have an autoimmune component. Stroke, burn patients, Parkinson's disease, cardiac disease, etc - again, inflammation. Hx of minor trauma, post-thoracic surgery, hyperlipidemia, drug-related. Dupuytren's contracture is also associated with increased risk. Possible genetic component
Pathophysiology of Adhesive Capsulitis
Synovial inflammation -> capsular fibrosis -> passive stiffness -> contractures of rotator interval and GH ligaments
Work-up for adhesive capsulitis
Plain films to rule out bone causes, MRI as well... But this is a clinical diagnosis of exclusion
Management of adhesive capsulitis
This will resolve on its own over 2-3 years. Tx is pain relief and corticosteroid injections so that the patient can tolerate PT, which is needed to restore mobility
MOI of ACL rupture
Usually non-contact: quick direction change, sudden deceleration, hyperextension, valgus, or tibial torsion. Patient will usually feel a pop. Women at greater risk after puberty because it changes the angle from hip to knee.
Felt a "pop," pain and swelling, sudden effusion within 10 minutes, decreased range of motion in a knee injury sustained in a non-contact sport
PE maneuvers to test ACL
Lachman's, pivot shift, anterior drawer tests
Imaging for suspected ACL rupture
XR to look for bony avulsions - usually normal, but a Segond's fracture is pathognomonic
MRI is gold standard and will show the ACL tear. The ligament will appear black. May also show contusions, indicating a pivot shift, which is also pathognomonic.
Arthrocentesis will show bloody fluid
ACL, MCL, and medial meniscus injuries
Management of ACL rupture
Refer to ortho surgery! Most common kind of graft is an autologous bone-patellar tendon-bone autograft. This provides greater stability but may cause some patients more anterior knee pain post-op. Could also do a hamstring tendon autograft but that might cause hamstring weakness.
MOI of MCL injury
Valgus force to knee, may or may not have twisted
Management of an MCL injury
Normally will heal well without intervention. May place in an immobilizer brace or a more functional brace, and range of motion exercises help as well. If there is laxity, suspect an ACL injury too.
Prevention of MCL injuries in football
MOI of patellar subluxation
Tenderness over medial patellar border, large and sudden knee effusion, and apprehension sign (involuntary quad contraction and dislike of lateral movement of patella)
Presentation of patellar subluxation
What not to miss in a high ankle sprain
Fibula fracture - if this fracture has mortise widening it's likely to require surgical repair
Avulsion fracture of 5th metatarsal on XR
NO fracture line in the space between 4th and 5th metatarsal
Don't miss diagnosis - fracture line is proximal to 4th and 5th metatarsal joints. Needs to be treated operatively with a fixation screw in athletes. Non-weight bearing for everyone. The challenge here is that it's in a watershed area so there's poor blood flow and therefore a risk of poor healing
What is the os coxa and when does it fuse?
Ilium, ischium, and pubis where they come together at the hip. Fuses at age 16, until then it's connected by the triradiate cartilage.
Types of cartilage in SI joint
Sacral side is hyaline, iliac side is fibrocartilage
Angle of femoral shaft relative to vertical axis. 13 degrees in males, 18 degrees in females
If you do arthrocentesis from the patellofemoral joint, are you sampling the tibiofemoral joint as well?
Yes since the synovial cavity is continuous
How are knee menisci tethered to the tibia?
Coronary ligaments made of fibrocartilage
Where is bone deposited in the growth plate?
Which ankle ligaments prevent over-inversion?
Anterior talofibular, posterior talofibular, calcaneofibular
Which ankle ligament prevents over-eversion?
Nerve roots for hip flexion
Nerve roots for hip extension
Nerve roots for knee extension
Nerve roots for knee flexion
Nerve roots for dorsiflex ion
Nerve roots for plantar flexion
Major extensors of the hip
Gluteus Maximus, posterior fibers of gluteus medius
Major flexors of the hip
Anterior fibers of gluteus medius, gluteus minimus, tensor fascia lata... And also iliopsoas
Superior fibers of gluteus Maximus, gluteus medius, gluteus minimus, tensor fascia lata
Adductors (among the butt muscles) of the hip
Gluteus Maximus... But the adductor muscles do most of this
Butt muscles that medially rotate the hip
Anterior fibers of gluteus medius, gluteus minimus, tensor fascia lata
Butt muscles that laterally rotate the hip
Gluteus Maximus, posterior fibers of gluteus medius
Lateral rotation contracting the piriformis could compress what nerve?
Nerve fibers in obturator nerve
Main dorsiflexor of foot
Lack of dorsiflexion
Foot drop, steppage gait
Blood supply to head and neck of femur
Medial and lateral circumflex femoral arteries
Blood supply to posterior compartment of thigh
Perforating branches of deep femoral artery
After the femoral artery passes through the adductor hiatus and into the popliteal fossa, the popliteal artery splits into what branches?
Anterior tibial artery and posterior tibial artery (which then gives off the fibular artery)
Dorsalis pedis artery comes from which artery?
Anterior tibial -> pierces interosseous membrane -> anterior compartment -> becomes dorsalis pedis
Medial and lateral plantar arteries come from which bigger artery?
Posterior tibial artery
What provides collaterals circulation around the hip?
Cruciate anastomoses - inferior gluteal artery, lateral and medial femoral circumflex arteries, first penetrating branch of deep femoral artery
Pre axial vein of lower limb
Great saphenous vein - drains into femoral at the femoral triangle
Post-axial vein of lower limb
Lesser saphenous vein - drains into popliteal vein
How do valves function in the deep veins of the leg?
Skeletal muscle pump means that they are closed when muscles relax and open when muscles contract
Most powerful dorsiflexor
What type of contraction does tibialis anterior do in the swing phase of the gait cycle?
Isometric/concentric contraction to dorsiflex foot and prepare for heel strike
What type of contraction does tibialis anterior do in the stance phase of the gait cycle?
Eccentric contraction to slowly lower foot to the ground and prepare for toe-off
Damage to which nerve produces a foot drop?
A nerve that can't re-establish organized nerve bundles after trauma might produce...
A post-traumatic neuroma
If you lose these muscles you can't run or jump
Gastrocnemius and soleus
Fibers proliferate around the third common digital nerve of the foot, compressing it and causing pain and paresthesias in someone who wears high heels
Describe pain sensation in neonates
Underdeveloped pathways, so have higher risk of hyperalgesia, immature respiratory centers so worse side effects from opioids, develop opioid tolerance more easily
Good ways to manage pediatric acute or procedural pain
Comfort position (lap, or sitting up), distraction, sucrose for infants under 6 months, breastfeeding for infants, don't reassure or apologize
Overall goals of pain management in kids
Minimize opioids, minimize side effects - might use scheduled NSAIDs, acetaminophen, opioids PRN
Analgesics that work via COX inhibition on arachidonic acid pathway
Analgesic that blocks central and peripheral prostaglandin synthesis
Acetaminophen - but avoid combo products like Vicodin or Percocet if possible, and give it IV/PO
Which opioid is especially contraindicated in children?
Is hydromorphone or morphine safer in renal failure?
Side effects of opioids and their management
Pruritus - nalbuphine, naloxone, ondansetron
Nausea/vomiting - ondansetron, metoclopramide
Respiratory depression - monitor for this, stop the meds, give naloxone
Acts on presynaptic calcium channels
IV lidocaine MOA as an analgesic
Anti-inflammatory, sodium channel blockade
NMDA antagonist, acts as an analgesic
Clonidine MOA as an analgesic
Alpha2 agonist, augments descending modulation
Why use regional analgesia?
Putting local anesthesia around a nerve - good pain control, reduced opioids, safer than epidural because there's less risk of ileus (and if it occurs it has a shorter duration)
What area of the spinal column do neuraxial blocks go into?
Meds go into the epidural space if they are done as an epidural, but a spinal block goes into the subarachnoid space (CSF) - more numbness for a shorter duration
What is the risk of a sympathectomy in a young patient under age 8?
Decreased blood pressure (all patients have a risk of urinary retention)
Which problem comes first in opioid use - sedation or respiratory depression?
Sedation always precedes respiratory depression
Analgesic ceiling effect
In NSAIDs, etc - beyond a certain dose you don't get improved analgesia
A patient on patient-controlled analgesia wants more meds -> how will you alter the dose if you need to?
Up the demand dose, but don't increase the basal dose
Are opioids better for acute or chronic pain?
Goals of treatment of chronic pain
Functional improvement at work, school, ADLs
Tools for chronic pain management that aren't meds
Patient education, CBT, DBT, mindfulness, coping skills, PT, OT, exercise, activity, treat comorbidities, improve sleep hygiene, diet, diabetes control, etc
Considerations for acetaminophen for chronic pain
Lower maximum daily dose
Considerations for NSAIDs for chronic pain
Watch for GI bleeds, renal function, cardiac issues
Which low-dose antidepressants can be used for chronic pain?
SNRIs (duloxetine, venlafaxine) and TCAs (nortryptiline, amitryptiline)
Which anticonvulsants are used for chronic pain?
Topiramate, gabapentin, pregabalin
Initial management of back pain without worrisome symptoms
Rest for a few days, ice/heat, NSAIDs, muscle relaxants, PT, acupuncture
When are epidural steroid injections beneficial for back pain?
May help with radicular pain or with facet joint or SI joint pain
What is a risk of doing spine surgery to resolve back pain?
May continue to have back pain after the surgery
Good prognosticators for epidural steroid injections
Education, radiculopathy, pain for <6mo
Bad prognosticators for epidural steroid injections
Constant pain, disrupted sleep from pain, unemployed due to pain
Presentation of facet joint pain
Mostly axial, often bilaterally, PE shows positive facet loading, paraspinal tenderness
Test for SI joint pain
Criteria to diagnose fibromyalgia
Widespread pain index: 19 areas, need pain in 4 or 5 areas over past week, and severity is judged by fatigue/waking up in refreshed/cognitive symptoms, and pain needs to have lasted for over 3 months
Management of fibromyalgia
NOT opioids. Anticonvulsants, dopamine agonists, SNRIs, TCAs, non-pharm management are good options
Painless mass between the tendon of the medial gastrocnemius and distal tendon of semimembranosus, right behind the medial condyle, driven by transient increase in intraarticular pressure
Dx of Baker's cyst
Ultrasound - may have internal septations, and is avascular (a vascular mass would suggest it could be sarcoma)
Management of Baker's cyst
Only aspirate if it's bothering the patient - treat with steroid injections if symptomatic or painful. 50% will recur.
DVT appearance on ultrasound
Common femoral vein has no flow or is full of stuff or doesn't compress well
Muscle strain appearance on MR
Bright on T2, focal mass with edema and contusion
Differentiate between schwannomas and neurofibromas
A schwannomas is a tumor of the Schwann cell. It is intrinsic to the nerve, better encapsulated, and easier to remove. A neurofibromas is a tumor of the nerve itself, is harder to remove, and has a worse prognosis. Treat both with surgical resection.
Benign, slow-growing fatty mesenchymal tumor that presents as a mobile, firm mass
PNS repair rules
Regrowth one inch per month
If cut, maximum repair is 70% of function
If patients are older than 40, nerve recovery decreases
2-3 cm nerve gap is the maximum that's feasible for good repair
Myelinated neurons in a fascicle are wrapped by ___.
Compression of nerves causes what change in signals?
Increased conduction time
One nerve injured
Multiple nerve injuries in different locations - in vasculitis, DM, lupus, sarcoidosis
Changes in central processing after irritation of PNS can cause what?
Chronic regional pain syndrome - pain, hyperalgesia, spasm
Nerve is bruised but intact
Nerve axon is transected
Endoneurial tube is transected and/or fascicles ruptured
Sunderland 1 nerve injury
Neuropraxia - localized, axons fine, conduction is preserved above and below injury. Recovery in minutes to 6-8 weeks - injury persists until local myelin repairs itself. Good prognosis
Sunderland 2 nerve injury
Axonotmesis - axon transected, Wallerian degeneration dismally, acute recovery may occur but proximal lesions heal better.
Sunderland 3 nerve injury
Endoneurial tube transected, Perineurium intact, Wallerian degeneration dismally, may form a neuroma
Sunderland 4 nerve injury
Fascicles ruptured -> scarring, axonal misdirection, reinnervation of inappropriate targets. Usually requires resection, repair, or graft. Will form a neuroma in continuity.
Sunderland 5 nerve injury
Nerve completely transected. Requires surgical repair. The proximal end forms a neuroma.
Cut axons degenerate distally
How long does it take the NMJ to die if a nerve is cut?
About a year
Why can't you get back 100% function with nerve repair?
Axons get narrower, so 100% function isn't possible
What's a procedure you can do to help prevent neuroma?
Embed the cut end of the nerve in muscle
Pain and numbness in lateral 3.5 fingers, worse at night, improved when shaking hands out or with wrist splints
Distal median nerve injury, like in carpal tunnel. There will be a sharp demarcation on the ring finger of the deficit. Positive Phalens test, Tinel sign. EMG will help show it. Tx is conservative.
Carpal tunnel with atrophy of thenar muscles
Surgical release of the median nerve
Proximal median nerve injury at the elbow presents with...
Benediction hand - weakness of long flexors of fingers, sensor loss in Palm
Pain from right elbow to medial two fingers, interossei weakness
Ulnar neuropathy - both palmar and distal surfaces may have pain. If there's dorsal involvement the injury is probably at the elbow, if not it's at the wrist. If long flexion is weak that localizes injury to the elbow.
Tx for ulnar neuropathy
Surg - simple decompression or transposition. Transposition is moving the nerve medially, which is used more for recurrences since it has a higher risk of complications
Pain and numbness of medial hand and little finger after writing
Hypothenar issue with ulnar neuropathy. Image here with MRI or US for ganglion cyst or Schwannoma. Treat conservatively or with decompression
R finger drop, radial deviation with extension (loss of ulnar extension)
Posterior interosseous nerve palsy - a high radial nerve palsy would give wrist drop, but just the PIN would spare the radial extensors.
Tx of PIN neuropathy
Have to release the Arcade of Frose to finish PIN decompression
L hand numbness with thenar atrophy and atrophy of first dorsal interossei, all one diagnosis
Thoracic outlet syndrome producing Gilliat-Sumner's hand, impinging lower trunk or medial cord of brachial plexus. Fix in surgery - make sure you don't hit the phrenic nerve!
Upper extremity weakness and fasciculations bilaterally with no pain or numbness
High suspicion for ALS
Shoulder pain, weak abduction and external rotation, prominence of scapular spine, atrophy of supraspinatus and infraspinatus
Supra scapular nerve entrapment in supra scapular notch... But need to rule out brachial plexus neuritis (severe shoulder pain without provocation followed by persistent weakness)
Most likely long thoracic nerve, spinal accessory nerve, or dorsal scapular nerve. Conservative to
R foot drop with decreased eversion but intact inversion
L5 radiculopathy or peroneal neuropathy
Decreased sensation of dorsal 1st web space
Problem with deep fibular nerve
Imaging for R foot drop
US or MRI to look for cysts, tumors, etc.
Tx for tarsal tunnel syndrome
Tarsal tunnel release - release each nerve!
Nerve trapped against iliac crest (lateral femoral cutaneous nerve) - obese patient or patient in really tight skinny jean, numbness of anterolateral thigh, worse with sitting. Tx with meds, weight loss, injection, surgery (would require snipping inguinal ligament)
Carpal tunnel EMG results
Prolonged latency for median nerve compared to ulnar nerve, drop in amplitude indicating axonal loss
Diabetic neuropathy EMG
Ulnar neuropathy nerve conduction study
Drop in velocity from above elbow to below, may also have decreased amplitude
M wave on EMG
Stimulation of muscle fibers
H wave on EMG
F wave on EMG
Supra maximal stimulation
Ptosis and miosis
Weak shoulder abduction
Axillary nerve injury
Can't make OK sign
Damage to anterior interosseous nerve (branch of median nerve)
Can't flex first two fingers
Can't extend last 3 fingers
Can't adduct 5th finger (Wartenberg sign)
Ulnar nerve problem
Pathophysiology of osteoarthritis
Initial injury to hyaline cartilage caused by its degeneration leads to a cascade of inflammatory response, causing increased breakdown, desiccation, loss of chondrocytes and their repair function, etc until there is no longer a smooth contour. Bone plate gets bony hypertrophy, synovial hypertrophy, inflammation, and osteophytes.
Imaging hallmarks of osteoarthritis
Non-uniform joint space narrowing from cartilage loss, subchondral sclerosis, osteophytes, subchondral cysts
Tests for nerve damage in little kids
Wrinkle test - skin won't wrinkle in warm water if there's a nerve injury
Sweat test - skin won't demonstrate typical sweat patterns
Pre-operative management if you are going to do a tendon transfer or nerve transfer
PT/OT - joint must be passively mobile. Pain management and social support also important.
Clinical indications for nerve transfer
Proximal brachial plexus injury, delayed presentation or referral, trauma causing segmental nerve loss, other trauma in that area
Principles for choosing a donor nerve
Purely motor, anatomically would be able to be removed without needing its own nerve graft, enough axons for the target muscle, has redundant function, has synergistic function with recipient nerve
Neuropathy with orthostatic hypertension
Neuropathy with skin rash
Neuropathy with skeletal deformities
Neuropathy with nerve enlargement
Neuropathy with abnormal hair and nails
Diagnostic test for large fiber neuropathy
EMG and nerve conduction study - look at amplitude, affected motor units
Diagnostic test for small fiber neuropathy
Autonomic testing, and skin punch biopsy in which you look at the density of intraepidermal nerve fibers to see if it's reduced
High A1c, hands and feet have neuropathy, slowly progressive with predominant sensory loss moving distal to proximal
Prodromal illness followed by tingling in hands and feet, ascending proximal and distal weakness, areflexia, due to Tcell driven response against peripheral myelin
Acute inflammatory demyelinating polyradiculopathy (Guillain-Barre syndrome, etc). LP shows increased CSF without WBCs. Tx with plasma exchange or IVIG
Neuropathy with increased IgM, heavy chains, or light chains
Length-dependent neuropathy with axonal pathology producing subacute combined degeneration of SC (corticospinal tracts, posterior columns, sensorimotor axonal polyneuropathy)
Vitamin B12 deficiency - test for B12 or methylmalonate
Copper deficiency neuropathy - what should you evaluate for?
Low vitamin B1 and neuropathy
Progressive sensorimotor axonal neuropathy in beriberi
Other toxins that can cause neuropathy
Alcohol, renal failure, heavy metals, chemo (vincristine, taxanes)
Early age of onset of neuropathy,, generalized, skeletal abnormalities, symmetric, slowly progressive
Most common is Charcot-Marie-Tooth - high arches, hammer toes. AD, develops in first 20 yrs of life
Sx of compartment syndrome
Decreased sensation in first web space - deep fibular nerve involvement
Pain with passive extension of toes, lower leg firm and tense
Pressures diagnostic of compartment syndrome
Delta P <30, or absolute P>30
Pain, pallor, pulselessness, poikilothermia, paresthesias, paralysis
Pathophysiology of compartment syndrome
Increased pressure -> ischemia -> ATP decreases -> cell death -> release of CK, myoglobin, muscle enzymes, electrolytes
CK levels posing greatest risk of rhabdomyolysis and AKI
CK > 15-25000
Factors important in muscle differentiation and repair
Myf5, MyoD, Mrf4