Ex 1 Wk 2 ORTHO Flashcards

Orthopaedics (342 cards)

1
Q

Role of orthopaedic surgery

  • definition
  • meaning
  • timeline
A
  • Surgical and non-surgical management of the musculoskeletal system.
  • Ortho = straight Paedis = child
  • Up until about 40 – 50 years ago, most orthopaedic treatment was non-operative
  • Now it is the treatment Arthritis, carpal tunnel, spinal stenosis, knee injuries, fractures, scoliosis, etc. (not just making a kid straight again)
  • Major subspecialties include Total Joints, Hand, Sports, Pediatrics, Tumor, Spine, Foot and Ankle, Trauma, Geriatric
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2
Q

How to do an effective orthopaedic physical exam

  1. what is most important diagnostic tool?
  2. what makes up most of physical exam (2)
  3. components of physical exam (6)
A
  1. HPI (History of present illness); The most important diagnostic tool is talking to the patient. Key points; age, duration, inciting event, specific location, previous treatment, expectations and goals.
  2. Physical exam; 98% is anatomy and biomechanics.
  3. Components of physical exam
    - Inspection; seeing is believing - have pt change to gown. check for Swelling, deformity, open wounds, masses, wrinkles, odors, bleeding
    - Palpation; odd bone movement, tenderness, what does it feel lik e- soft, smooth, hard, mobile, crunchy?, temperature - warm, clammy, blanching? Neurovascualr exam
    - ROM; passive and active. any restrictions, crepitation, apprehensions
    - Strength; weakness due to pain or true weakness?, grade 1-5 (No 0)
    - Neuro; reflexes? sensation?
    - Special tests; body part specific
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3
Q

Most important diagnostic test in orthopaedics

why ?

A

X-RAY

  • Reading the X-rays will give you a better understanding of the fracture, the fixation, and what you can do to it.
  • It will allow you to see if there are any changes in the fixation

**Look at it yor self. Trust no one

  • NEVER look at films before H&P –May cloud your physical exam
  • Use your history and exam to guide you
  • Get the right films (minimum 2 views at 90 degrees to each other)
  • Don’t accept poor films –Centered on injury
  • X-ray joint above and below injury
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4
Q
  1. what can you see on X-ray?

**2 classes (3 each)

A

•Radio-opaque items

–Bones

–Some soft tissues

–Hardware

•Radio-lucent items

–Air

–Sutures

–Ligaments

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5
Q

Tips of reading X-ray

  • Check what 2 things to prevent mistake
  • What views are you seeing? (3)
  • Skeletally mature or immature?; old or young pt
  • What bone is involved?; term for bone in hand? feet? what bone has many promineses? prominences?
  • What part of the bone is involved?; bone divided to what 3 parts
  • Fracture type?; what fx require lowest energy? highest energy? poorly tolerated? how many view to see dislocation?
  • Does it involve the joint?
A
  • Check the person’s name and date on the film
  • What views are you seeing? (AP, lateral, oblique)
  • Skeletally mature or immature; mature has no growth plates. you see immature in kids (growth plates present)
  • What bone is involved? e.g metacarpals in hand, matatarsals in foot. scapula has many prominences (glenoid, coracoid process, acromion, spine). Tibia or fibula (not tibular/fibia)
  • What part of the bone is involved?; long bone fractures described by dividing bone into 3 (EMD) - epiphyseal, metaphyseal or diaphyseal. Is it intraarticlar?
  • Fracture type?; transverse, obliqe, spiral (lowest energy reqired) , comminuted (highest energy required). Displaced, anglation, rotation (twisted along axis of bone) - rotational malunion is poorly tolerated**. Dislocation - you need 2 views to see a dislocation (whether it was anterior or posterior)
  • Does it involve the joint?
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6
Q

Describe the fracture

A

AP and lateral view of an ankle in skeletally mature individal with displaced communuted intraticlar fracture of the distal tibia

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7
Q

Trama evalation

ABCs

A
  • Airway – speaking??
  • Breathing – intubate?
  • Circulation – PULSE, stable BP? vascular access?
  • Disability – can patient move extremities?
  • Expose – clothes come off, and patient is inspected
  • Fix dinner……
  • Go to movie……
  • Orthopaedics; It is not “OMG, there’s a fracture, call orthopaedics!!”**It is not a life threatening emergency in the first hour
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8
Q

When examining trauma patient, what is the first thing to get if patient is conscious

A

HISTORY (for conscious patient)

  • Sometimes hard to get from the patient – most should be known by the time Ortho is involved
  • Mechanism (history)
  • Medical Hx/surgical Hx
  • Medications/allergies
  • Social: drug use, tobacco, EtOH, vocation/education/social
  • Pertinent ROS: neurologic, musculoskeletal, constitutional, mental
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9
Q

To examine trauma patient ; what must you do?

**3 standard x rays for trauma

  • what is gold standard to dx fracture
  • what 2 actions will clear soft tissue c-spine? exception?
  • what do you do for joint fractures
  • pelvis/acetabulum?
A
  • H&P is important
  • You need to touch your patients. Start from head and work your way down
  • 3 xrays for standard trama; lateral C-spine, chest, pelvis. • PALPATION and MOTION clear soft tissue c-spine as long as there are no distractions (like long bone fraccture)***

**XRAY IS GOLD STANDARD OF FRACTURE DIAGNOSIS; Get the joint above and below the fracture – always!!

  • Joint fractures get CT’s
  • The pelvis/acetabulum gets a CT with thin cuts; If hip is dislocated, CT after the hip is reduced
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10
Q

Routine xrays

**what is recommended with hip dislocation or acetabular fracture

A
  • X-ray (routine):
  • C-spine – going the way of the dodo
  • CXR – still popular
  • A/P pelvis – forever and always!. Acetabulum – Judet views (with rotation if possible). Pelvic ring – inlet/outlet views

**Hip dislocation or acetabular fracture - CT with thin cuts and reconstructions AFTER the hip is reduced.

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11
Q

Upper extremity exam (4)

A
  • Brachial Plexus (C5-T1); Associated injury patterns
  • Vascular (sbclavian, axillary, brachial, distal radial/ulnar)
  • Soft tissue integrity
  • Peripheral nerves; Median, Radial, Ulnar

**Know the 30 second upper extremity evaluation

**Unconscious – be aware: Expanding hemtoma – ST disassociation or The “compartment syndrome” (next talk)

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12
Q

Devastating injury of upper extremity and can be fatal

  • can’t move arm - you think it’s clavicle fracture but it’s not

**Can bleed to death

A

Scapulothoracic disassociation

  • Devastating and often missed initially!
  • Alert patient who can’t feel/move UE
  • Check the vascular status! Expanding Hematoma!!. Hypotension can soon to follow – and be too late
  • Beware “The Clavicle fracture” in the intubated patient
  • Arterial findings may be your first (only) clue!
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13
Q

Exam of upper extremity

Brachial plexus

pre vs post ganglionic

A
  • Pre-ganglionic – nerve root avulsion – dismal prognosis
  • Motor Cycle
  • Rough OB Doc
  • Post-ganglionic – repair…
  • Penetrating injuries
  • KSW
  • GSW
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14
Q

what part of lower extremity

  • Crush vs. Open book: hemorrhage is the main acute issue! Open book >> lateral compression
  • Need x-ray
  • Close the book if hemodynamically unstable– the sheet works well in the emergent situation. Then it’s either embolization or…….ligation
A

Pelvis

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15
Q

identify nerve of lower extremity

  • if you loose this nerve you will feel numb but can still walk

**2 branches

  • what branch can you injure in posterior hip dislocation vs knee dislocation \
  • which branch can cause foot drop
A

Sciatic nerve; if you loose this you will be numb but can still walk. if yo loose femoral you can’t walk

A. Peroneal branch

  • More likely to be injured in posterior hip dislocations than tibial branch
  • Nightstick injuries to the proximal fibula – foot drop

B. Tibial branch

  • Knee dislocations
  • Penetrating injuries
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16
Q

Identify Nerve of lower extremity

  • can result in Anterior hip dislocation
  • if you loose this nerve you can’t walk

**is this nerve the most lateral or most medial compared to iths artery, vein counterparts?

A

Femoral Nerve

  • Antigravity muscles of the leg
  • Damaged in penetrating trauma and iatrogenically. Remember “NAVEL” (nerve, artery, vein, lymphatics: lateral to medial)
  • Anterior hip dislocation
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17
Q

Vasculature of lower extremity

**Hip vs knee dislocation

**If pulse is okay, does that mean you don’t have compartment syndrome ?

A
  • Femoral; anterior hip dislocation
  • Popliteal; anterior and posterior knee dislocation
  • PT;
  • DP

**Good pulse is not an indication that compartments are okay

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18
Q

Systemic approach to reading plain radiograph (5)

A
  • Type of x-ray
  • Radiographic age of patient (mature or immature)
  • Views
  • What is wrong…..What is right?
  • A fracture requires an x-ray of one joint above and below
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19
Q

facts of child absue

  • age
  • common fractres
A

Child abse with fracture (multiple with different stages of healing)

A. Age; under age 3. mortality rate may be as high as 50%

B. Common patterns of abse; unwitnessed spiral fractures

C. common fractres

  • rib fractures: the most commonly found fractures in child abuse (followed by humerus, femur, and tibia);

- Femur fxs: the majority of femur fxs in infants are due to abuse (non-ambulating)

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20
Q

differential dx of child with fracture (4)

A

A. Normal

B. Abuse

  • Inconsistent stories
  • The child’s demeanor/caretaker’s attitude toward the child and medical personnel
  • Above patterns

C. Osteogenisis Imperfecta (OI)

  • Family history
  • Blue sclera (type one collagen, glycine substitution – bone, tendon, skin)

D. Infantile Disease Cortical Hyperostosis (Caffey’s disease)

  • Jaw involvement
  • Resolves by age one usually
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21
Q

child with a fracture

**Not usually abuse (5)

A
  • Toddler’s Fx of the tibia; can’t bear weight
  • Torus or “buckle” fracture (wrist)
  • Crushed fingers
  • Nurse maids elbow; pull kid’s hand up

Skull fracture in ambulatory child….

Spiral fracture – twist

  • Proximally and distally
  • In kids that just start walking
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22
Q
  • Hx:
  • 6 y/o female who was driving her 4 y/o sibling on an ATV, drove into the road and was struck by an auto
  • PE:
  • Badly swollen left thigh, leg, and foot – tight. Mild ecchymosis over thigh. Prominent bulge over left anterior inguinal canal
  • excellent distal pulses.
  • LLE shortened and EXTERNALLY rotated
A

Compartment syndrome - bad example of x-ray

New X ray of Hip - Dislocation of hip in child (looks like compartment syndrome). No acetabular fracture.

Correct presentation; •I have a 4y/o female trauma patient who was involved in an ATV vs Auto collision – she was driving the ATV and sustained an impact injury to her left lower extremity. Trauma has seen the patient and she has been cleared with an isolated anterior left hip dislocation. In addition she has a mass in the inguinal region – possibly the femoral head - and a contused/ecchymotic tightly swollen thigh with no radiographic evidence of other lower extremity fractures. She has good distal pulses, and appears sensate grossly in all dermatones distally as well. I am concerned about the hip and the thigh swelling, and trauma is thinking about emergent fasciotomies….”

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23
Q

Definitions

  1. fractured bone
  2. comminuted
  3. Non-union
  4. Osteomyelitis
  5. Neurovasclar injury
  6. compound fracture (old terminology)
A
  • Fractured bone = broken bone
  • Comminuted – many pieces
  • Segmental – segmental (broken in many places?)
  • Non-union – failure of fracture to heal
  • Osteomyelitis - bone infection
  • Neurovascular injury – compromise of the vascular or neurological status of the affected limb

¨Old terminology (but correctly used): Compound fracture – Open fracture

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24
Q

Definition

1 involves a break in the overlying skin that leads to direct communication between the fractured bone and the environment in which the injury occurred - this communication results in contamination and the potential for (bone) infection.

any fracture with overlying or adjacent skin compromise (sub-Q fat) is an open fracture until formally explored (in the OR) and shown to be otherwise.

  1. compromise or loss of perfusion distal to the site of injury – pulses + capillary refill vs. CR only vs. cold ecchymotic limb
A
  1. Open Fracture
  2. Vasclar injury
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25
Definition ORIF Ex-fix Reduction CR NV IMN
* ORIF – open reduction internal fixation * Ex-fix – external fixation * Reduction – setting the fracture and aligning the parts. Also relocating dislocated joints * CR – capillary refill * NV – neurovascular (intact) * IMN - Intramedullary nailing
26
Definitions 1. any fracture around a joint with extension of the fracture into the joint space and particularly into articulating cartilage 2. Femur, tibia, humerus, forearm; practically speaking this is applied to lower extremity fractures
1. Intraarticular fracture 2. Long bone
27
Emergencies - what is this? * a rise of interstitial pressure within a confined space (muscle within fascia envelope) resulting in a failure of perfusion at the micro vascular level causing ischemia of the myoneural tissue * Happens with or without a fracture * Most common in the **“leg”** * A true (ortho) emergency \*\*what 2 are not good indicators that you do not have the condition ? \*\*Number 1 clinical sign?? \*\*\*\*
**Compartment Syndrome ;** perfusion issue - pressure rising in tisse, build up lactic acid, muscle starts dying and nerve also die. _Pulses not a good indicator_ because you can still get perfusion in some areas (distally?) * – An injured limb with tight “compartments” and ischemia * Often intractable pain with a tense limb (you don’t have to wake them to ask if it hurts) * Clinically: **pain** **out of proportion** with passive or active motion (dramatic) – very specific \*\*\***Number 1 clinical sign** * Objectively: interstitial compartment pressure above a set amount (different criteria) - sensitive * **_Pulses_ and _capillary refill_ are NOT an indicator of compartment syndrome**
28
Emergencies; life or limb \*\*give examples of absolute (5) vs relative emergencies (4) \*\*when can a relative emergency become an absolute emergency
A. **Absolute Emergencies (immediate)**: * Open fractures * Compartment Syndrome * Vascular compromise * Dislocations with neurovascular compromise * Hip (femoral neck) fractures in the young (\<50 years old) B. **Relative Emergencies (within 12-24 hours)** * Open fractures…… * Femur fractures * Dislocations without neurovascular compromise (only if for good reason) * Pediatric elbow fractures (supracondylar; **emergent if neurovascular compromised**)
29
identify class of condtion * Not emergent, but…. * Supercondylar elbow that is well perfused….?? * Geriatric hip fractures where hip replacement is the treatment– ASAP per medical status (**these patients typically are as healthy as when they hit the door**), BUT WHY DID THEY FALL?? * Tibia (closed and without compartment syndrome) * Any fracture combination that is limiting mobility
**URGENCY** - not emergency \*\*Patient has a **FALL**
30
treatments 1. what you need for every open fracture 2. when fecal matter is involved 3. compartment syndrome?
1. Every open fracture should get **NSAID.** **-** Essential first step is initiation of _systemic abx_ (before leaving ER - type used is based on nature of wound), _surgical debridement_, _stabilization_ (ex-fix or ORIF). 2. **Penicillin** – when you have **fecal matter** involved (prevent complication of C-diff – GAS gangrene and megacolon – pseudomembranos colitis) 3**. Compartment syndrome**; **Emergent compartmnet release** - cut open the skin and fascia - complete release of surrounding fascia - do it within 8hrs of symptom onset - remove any restrictive items (bandage, casts, etc) A. _Emergent compartment release_; Complete release of the surrounding fascia, Need to be done within 8h of symptom onset, Be sure it’s not from restrictive bandages, casts, or other tight material surrounding the limb B. Stabilization – usually _ex-fix initially_ (if associated with a fracture) C. Definitive _fixation at closure or with skin grafting_
31
5 P's of Ischemia \*\*What is most important P in compartmnet syndrome?
* Pain * Palor * Parasthesia * Pulse (less) * Poikilothermia \*\*Pain is the most important in compartment syndrome, then dysthesia – the others tend to be late findings
32
4 C's of muscle viability \*\*What fractures get surgery
* Color * Contractility * Consistency * Capacity to bleed \*\*\*Fractures that get surgery, open fx, multiple fx, (polytrauma), intraarticular fx, femur fx, both bone forearm fx in adults, severely displaced/mal-aligned after attempted reducton (unstable fx), non-unions/mal-union (poor healing)
33
Upper extremity \*\*Identify * **High energy marker** * Risks: Associated injuries at 50%– rib fractures, great vessel injury, brachial plexus injury, pulmonary/cardiac contusion, pneumo/hemothorax * Temporization: Comfort * Definitive care: **Sling with early mobilization.** Rarely surgery - if severely displaced or into the glenoid
SCAPULA
34
Upper extremity - \*\*Identify * Risks: **Mal/non- union** * Temporization: Comfort * Definitive care: **Sling or figure-8 bracing with early mobilization**. Rarely surgery if severely displaced or shortened (2 cm), or non-union \*\*\*What is a VERY SEVERE COMPLICATION that occurs that is confused with this?
CLAVICLE * Be aware of **ST disassociation! •ST=scapulothoracic** * Clavicle and/or scapular fractures in a male with a motorcycle “event” * The “nerve root avulsion” (downward traction on the shoulder)
35
Upper extremity - \*\*Identify \*\*can take a lot of crap 1. Risks: * Acute – radial nerve injury * Chronic – non-union 2. Temporization: * Symptomatic pain control * **Sling/immobilization without compressing fracture** **\*\***Identify options for definitive care (when do you use ORIF?)
HUMERUS * Fracture brace early * ORIF only if **polytrauma, displaced, non-union and certain cases neurovascular compromise** * Early shoulder motion
36
UE - Forearm \*\*Identify risks (2), temporization and definitive care (2)
**Risks:** * Acute - compartment syndrome or NV compromise * Chronic – functional loss from poor reduction **Temporization:** •Long arm splinting and comfort **Definitive care:** * Radius and both bone fractures are typically operative cases (adults) * Ulna alone – splint if non-displaced, o/w ORIF •
37
LE; Pelvis/acetabulum - marker for? - identify risks, temporization and definitive care?
Marker for **high energy trauma** **Risks:** * Acute – Bleeding (pelvic ring)! * Long term - DJD, Sciatic nerve/lumbar/sacral plexus injury, marker for other injuries….. **Temporization:** •Traction, external fixation, pelvic sling/sheet **Definitive care:** •Typically operative with displacement or instability
38
identify condition \*\* \*\*What is the treatment
**HIGH RISK PELVIC DISRUPTION** lacerate any of these arteries lead to **bleeding to death** - Patiens with pelvis fractures can die. pelvic fractures can be hard to understand. Treatment is percutaneous fixation
39
Identify lower extremity * **Marker for high energy trauma** * **Risks:** * Acute – cardio-pulmonary compromise * Non-union, pain, infection * **Temporization:** * Traction or ex-fix (traveling traction) * **Definitive care:** * Intramedullary nailing (IMN), ex-fix \*\*\*Summarize 3 markers for higher energy trauma in the extremities
FEMUR \*\*Marker for high energy marker in extremities - **Scapula, pelvis/acetabulum and femur**
40
identify lower extremity fracture **•Risks:** * Acute – like to be open, compartment syndrome, NV compromise * Chronic – mal-non union, osteomyelitis with open fractures, amputation **•Temporization:** * Splint * Ex-Fix **•Definitive care:** * Stable patterns can still be casted * Most are fixed with IMN or ex-fix
TIBIA/FIBULA
41
LOW ENERGY MECHANISM - arise from what in elderly? - types of fractures (6) - what is a pathologic condition?
•Most elderly fractures arise from simple falls – must determine why!! Low energy patterns - the so-called “fragility fractures * The “FOOSH” – fall on out-stretched hand resulting in the distal radius fracture * The elderly “hip fracture” * The LC-1 pelvic ring fracture FFSH * The elbow or proximal humerus fracture * The “knee fractures” * Periprosthetic fractures * Osteopenia/osteoporosis is a pathological process \*\*Must be addressed!!!
42
Anatomy of hand - identify 3 joints in hand - 1 joint in feet
1. Hand joint - Distal interphalangeal joint **(DIP)** - Proximal interphalangeal joint **(PIP)** - Metacarpal phalangeal joint **(MCP)** 2. Foor joint Foot MTP: Metatarsal phalangeal joint
43
identify joint condition **Degenerative joint disease DJD** - primary vs secondary (which is from aging? which is from repeated joint injury?) \*\*what is best treatment and prevention
**Osteroarthritis;** best treatment and prevention is to **loose weight** •“Degenerative joint disease” DJD 1. Idiopathic (primary) with **aging** * Men: Hips predominate * Women: Knees and hands predominate 2. Secondary * _Repeated injuries to a joint_ * Hemochromatosis * Obesity
44
osteoarthritis - condition - phases
A. Degeneration of cartilage outpaces repair * 80-90% by age 65 * Mechanical defects eg muscle strength, obesity B. **Phases:** * Chondrocyte injury * Chondrocytes proliferate * Chondrocyte drop out with loss of cartilage
45
* Superficial roughened and cracked cartilage * Bone eburnation (exposed bone on surface) looks like polished ivory and underlying bone sclerosis * Joint mice (loose bodies of cartilage) * Subchondral cysts of synovial fluid * Osteophytes (bone spur): Extra bone at joint edge \*\*\*\*\*Presentation to this degenerative joint disease (7); pain type, stuff when?, pain worse when? what is seen at DIP in women? what is found at joint (sound) ROM what impinge on nerve roots?
Osteoarthritis A. Insidious typically involving one or a few joints * Deep achy pain * Morning stiffness **•Worse with use** * Crepitus of joint * Limited range of motion * Vertebral osteophytes impinge on nerve roots B. **Heberden nodes**: Osteophytes at **DIP** in **women**
46
Areas affected in osteoarthritis (7) Areas spared (3) \*\*remember that osteoarthritis is a degenrative joint disease so we talking about joints here
OSTEOARTHRITIS Areas affected; Hips, Knees, Lower lumbar, Cervical, DIP, PIP, First Carpometacarpal joints SPARES: wrists, elbows, shoulders joints
47
Identify condition in picture
Osteophytes - bone spore (**Osteroarthritis**) \*can be in DIP joint in women - called Heberden's Nodes
48
Identify joint condition * Systemic autoimmune inflammatory disease * Nonsuppurative **(no pus) proliferative inflammatory synovitis** often **destroying cartilage with later ankylosis of the joint** * Female \> Male * Age: Any but most often 40-70 * Some genetic susceptibility \*\*what is the major clinical indicator? (in picture) \*\*Most common cells found?
RHEUMATOID ARTHRITIS * **PANNUS**: Exuberant inflamed synovium * **Chronic inflammation** with T-cells (**mostly CD4+**), B-cells, plasma cells, macrophages * Granulation tissue with hemosiderin * Erodes articular cartilage * Erodes bone: Juxtarticular cysts/damage, Subchondral cysts, Osteoporosis
49
pathogenesis of rheumatoud arthritis - 2 types of antibodies foremd (which is specific? non-specific?) - 2 components of synovial fluid (high vs low)
A. Pathogenesis: * Ag exposure in a susceptible host creating an ongoing autoimmune process * 80% have **Rheumatoid Factor** (autoAb against Fc portion or IgG) but is not specific * **Ab to Citrullin-modified peptides** (anti-cyclic citrullinated peptide or CCP Ab) more specific * TNF major role B. Synovial fluid: **High protein content (indicate inflammation), low mucin content,** inflammation
50
identify joint condition * Clinical course variable * Can have **periods of remission** * 10% acute onset but most insidious * May be preceded by malaise, fatigue, myalgia * **Symmetric** with small joints before large * PIP, MCP, MTP (note OA is DIP) * Later wrists, ankles, elbow, knees (spares hips) * Joints: **Swollen, warm, painful and stiff with _inactivity_** \*\*must present with 4 of what presenattaions?
RHEUMATOID ARTHRITIS
51
identify joint condition \*\*Flexion-hyperextension of fingers (**swan neck; boutonniere**) -other presentations on xray (3)? 3 others
**RHEUMATOID ARTHRITIS** A. X-ray: * Juxta-articular osteopenia * Bone erosions with narrowing of joint space from loss of articular cartilage * Joint effusions B. Radial deviation of wrist C. Ulnar deviation of fingers D. Flexion-hyperextension of fingers (**swan neck; boutonniere**) E. Synovial cysts - Baker cyst (back of knee)
52
Identify condition in Rheumatoid arthristis * Most common cutaneous manifestation (25%) * Areas subject to pressure: ulnar aspect of forearm, elbows, occiput, lumbrosacral * Fibrinoid **necrosis surrounded by macrophages** (granuloma)
Rheumatoid nodules
53
what condition that occur in rheumatoid arthristis affect blood vessels
**Vasculitis** •Does not involve kidneys * Can be obliterative endarteritis of vasa nervorum and digital arteries * Neuropathies, ulcers, and gangrene * Leukocytoclastic venulitis * Purpura, skin ulcers, and nail bed infarction **May be adjacent tendonitis, myositis**
54
identify joint condition * Heterogeneous group by definition before age 16 and present 6 weeks * Oligoarticular \< 5 joints * Polyarticular * Systemic * Knees, wrists, elbows, ankles (large joints) \*\*\*Identify extra-articular manifestations (6)
JUVENILE IDIOPATHIC ARTHRITIS Extra-articular manifestations: **pericarditis, myocarditis, pulmonary fibrosis, uveitis, glomerulonephritis, growth retardation**
55
how is JIA different from RA \*\*differences vs similarity - oligoarthritis mroe common where? sytemic onset? which involve large joints? RF absent or present? rheumatoid nodules? antinuclear antibodies (ANA)? \*\*2 similarity
**JIA** differs from RA * Oligoarthritis is more common * Systemic onset more common * Large joints * Absence of rheumatoid factor * Absence of rheumatoid nodules * May be ANA positive **Same as RA** * Pannus formation * Morphology of involved joints
56
Identify joint condition * Pathology in ligamentous attachments Immune mediated; **no specific autoantibody** * Many are **+ HLA B27** **Rheumatoid factor NEGATIVE** \*\*4 examples
**Seronegative Spondyloarthropathies** 1. Ankylosing spondyloarthritis 2. Enteritis-associated arthritis (IBD) 3. Reactive arthritis (reiter's) 4. Psoriatic arthritis \*\*\***PAIR** ACRONYM
57
Identify condition **•Young adults**; **M**\>F. Onset 2-3 decade with **low back pain** •HLA B27 (90%) **•Axial joints; Sacroiliac joint.** Apophyseal joints of vertebrae \*\*Identify - inflammation of - complications? (5) \*\*\*What does the X-ray show
**Ankylosing spondylitis** \*\*Xray show Frontal view of the lumbar spine demonstrates the classic **"bamboo" spine of ankylosing spondylitis** due to **bridging syndesmophytes.** Syndesmophytes of the entire visualized spin, ligamentous ossification (especially supraspinous and interspoinous ligaments), and sacroiliac joint ankylosis. **•Inflammation of tendon/ligament insertion;** Ossification of inflammation. Fibrous and boney _ankylosis_ •**Complications**; - 1/3 hip, knee, shoulder arthritis - Uveitis - Aortitis - Amyloidosis - Spine fractures
58
identify joint condition * Appendicular noninfectious arthritis * \< 1 month after primary infection * Genitourinary: Chlamydia * GI: Shigella, Salmonella (diarrhea) * **Triad?** **\*\*What cause sausage toe or finger?** \*\*lower extremity in symmetric or asymmetric pattern?
REACTIVE ARTHRITIS (REITER SYNDROME) **Arthritis** **Urethritis or cervicitis (nongonococcal)** **Conjunctivitis** **\*\***can't see, can't pee, can't skii * 20-30s * HLA B27 (80%); some HIV * Ankles, knees feet (lower extremity) in asymmetric pattern * **Sausage toe or finger** from digital tendon sheath synovitis •
59
identify extra-articular problems with reiter syndrome
Extra-articular * Balanitis * Conjunctivitis * Heart conduction defects * Aortic regurgitation * Symptoms wax and wane with 50% recurrence
60
\*\*Identify joint condition * occur after primary GI infection by Yersinia, Salmonella, Shigella, Campylobacter * Liposaccharide stimulate immune response * Most often abrupt in knees and ankles * Generally clears in \< 1 year
ENTERITIS-ASSOCIATED ARTHRITIS
61
identify joint condition * HLA- B27 and HLA-Cw6 * Onset 30-50 * Insidious \> acute onset; peripheral and axial * 50% asymmetric in **DIP** of hands/feet * **Pencil in cup deformity** * Can affect large joints * Can cause sacroiliac and spine disease
PSORATIC ARTHRITIS \*\*10% in psoriasis patients
62
Identify condition Bacterial almost always suppurative * Hematogenous spread is most common * \< 2years: H influenzae * Adolescent/young adult: Gonococcus (F\>M) * Elderly and children \> 2 years: S auerus * Sickle cell disease: Salmonella \*\*Identify presentatin with bacteria (predisposing conditions, what is swollen? GC, drug abuse?)
INFECTIOUS ARTHRITIS Bacterial * Predisposing conditions: Immunodeficiency, abnormal joint, debilitation, iv drug abuse, arthritis * Swollen hot joint * GC: Often subacute * One joint: Knee \> hip \> shoulder \> elbow * Drug abuse: Axial joints
63
conditions with infectious arthritis (3) \*\*\*Where do you see **Borrellia burgdofreri (cockscrew image)?**
**1. TB (tuberculosis)** * Monoarticular typically from adjacent osteomyelitis or hematogenous spread * Vertebrae, hips, knees ankles **2. Viral** * Parvovirus B19 * HCV, HBV * HIV **3. Lyme disease - Borrellia burgdofreri (cockscrew image)** * 2 weeks – 2 years after bite from _Ixodes_ * 60-80% of untreated; prominent in late disease * _Remitting/migratory arthritis_ in large joints knees \> shoulders \> elbows \> ankles * Chronic synovitis with organisms near vessels
64
identtify condition * Uric acid from purine metabolism. Crystals are negative birefringent * End point of hyperuricemia * Acute arthritis from monosodium urate precipitation in joint, can become chronic * Tophi: Mass deposits of urates * Urate nephropathy common if chronic \*\*2 types - condition/problem
GOUT * 10% population has hyperuricemia. Gout in 0.5% of this population * Primary gout (90%):Unknown cause (90%). Known enzyme defects (eg partial HGPRT) * Secondary Gout\*\*\*; Increased nucleic acid turnover eg AML (treat gout before giving chemo). Chronic renal disease \*\*HGPRT (Hypoxanthine guanine phosphoribosyl transferase) is a salvage enzyme for purine metabolism Defect increases de novo production
65
Gout - what precipitates? - is it an arthritis? \*\*What 3 things indicate gout?
1. **Monosodium urate precipitates** from supersaturated synovial fluid * Negative birefringence * Precipitates better at lower temperatures * Crystals initiate acute and chronic inflammation * Dissolve over time and symptoms abate 2. **Acute arthritis** joint aspirate samples need to be polarized for crystals and cultured \*\*\***Hot first toe** almost always indicative of gout (also **negative birefringent**, **tophi**)
66
Identfiy gout phases (4)
* Asymptomatic hyperuricemia * Acute arthritis; 50% First MTP joint foot. Instep \> ankles \> heels \> knees \> wrists * Intercritical gout: No symptoms * Chronic tophaceous gout
67
* **Pathognomonic of gout** * Large deposits of urate * Macrophages, lymphocytes and giant cells **•Location** * Tophaceous Arthritis: * Joints and periarticular tissue * Inflammation destroys synovium, joint and adjacent bone * Skin, soft tissues and organs
TOPHI
68
Risk factos of gout (6)
* \> 30 years (ie duration of hyperuricemia) * Genetic predisposition * Heavy drinking * Obesity * Drugs eg thiazides * Pb toxicity
69
* “Pseudogout” or “chondrocalcinosis” * \> 50 years; increases to 50% at 85 years * Usually asymptomatic * Mimic other forms of arthritis * Acute, subacute or chronic * Knee \> wrist
CALCIUM PYROPHOSPHATE CRYSTAL DEPOSITION DISEASE (CPPD)
70
* \< 2 cm cyst near joint or tendon sheath * Wrist is most common * Cystic or myxoid degeneration of tissue * No communication with joint space
Ganglion Cyst
71
identify •Connected to a joint capsule or bursa **•** cyst often in setting of Rheumatoid Arthritis
Synovial cyst
72
* t(1;2): Express CSF-1, attract macrophages * Classification: 1. Diffuse (Pigmented Villonodular Synovitis) 2. Localized (Giant Cell Tumor of Tendon Sheath) * Macrophages and giant (macrophage) cells * Hemosiderin and lipid vacuoles
TENOSYNOVIAL GIANT-CELL TUMOR
73
**Pigmented Villonodular Synovitis (PVNS)** * Joint synovium diffusely affected * Red/brown to yellow from **hemosiderin** * Lush villous surface * 80% knee **•Locking or swelling**; later decrease range of motion * Can erode bone and create a mass * Often recurs after excision
DIFFUSE TENOSYNOVIAL GIANT-CELL TUMOR \*\*hard to get rid off. usually reoccur \*\*Shag carpet villi
74
* Well circumscribed * Often attached to synovium or tendon * Slow growing painless * Fingers and wrists (**Most common soft tissue tumor of hand; especially _fingers_**)
LOCALIZED TENOSYNOVIAL GIANT-CELL TUMOR \*\*soft tissue mass in finger
75
Give examples of soft tissue tumors
* Fatty (Adipose tissue) * Fibrous * Fibrohistiocytic * Skeletal muscle * Smooth muscle * Vascular * Peripheral nerve * Tumors of uncertain histogenesis
76
General principles of soft tissue tumors - which is more in numer (benign or malignant?) - metastasis - what parts of body? - most common cause? - Associations
* Benign outnumber malignant at least 100:1 * Metastasis tend to be “blood born” to lungs, liver, bone * 40% lower extremity; especially thigh * 30% trunk and retroperitoneum * **Bone involved by direct extension or metastasis\*\*\*\*\*** * MOST COMMON cause is unknown * Associations:Radiation (predispose to sarcoma),Trauma eg post mastectomy: Angiosarcoma, Human Herpesvirus 8: Kaposi’s sarcoma, Chemical exposure,Thermal burns. \*\*Anything that create lots of inflammation
77
Identify genetic syndromes (4) 1. malignant peripharal nerve sheath tumor 2. Fibromatosis (desmoid) Colon polyps, osteomas, epidermal cysts, dental abnormalities, duodenal and thyroid cancer Defect includes tumor suppressor gene APC 3. soft tissue sarcoma and other malignancies 4. telangiectasias over skin and mucosal surfaces
1. Neurofibromatosis type 1 •Malignant peripheral nerve sheath tumor 2. **Gardner Syndrome** •Fibromatosis (desmoid) 3. **Li-Fraumeni Syndrome (mutant p53)** •Soft tissue sarcoma and other malignancies 4. Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu Disease) •Telangiectasias over skin and mucosal surfaces
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Tumor genetic changes \*\*translocations and fusion gene 1. Ewing sarcoma and primitive neuroectodermal tumor 2. Liposarcoma - MYXOID and ROUND CELL type 3. Synovial sarcoma 4. Rhabdomyosarcoma - ALVEOLA type 5. Extraskeletal myxoid chondrsarcoma
Picture
79
What type of tumor is this?
Tumor that big is **Sarcoma** (soft tissue) \*\***Soft tissue** sarcoma - **barely touching bone, color variation**
80
General principles of soft tissue sarcoma - most common in children vs adults
* 15% arise in children * Rhabdomyosarcoma in **children** * Synovial sarcoma in **young adults (20s - 40s)** * Undifferentiated pleomorphic sarcoma (malignant fibrous histiocytoma) and liposarcoma in **mid to late adulthood**
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Prognosis of sarcoma \*\*3 things affect prognosis
1. Type (recapitulation of tissue type) 2. Stage (location and size) •Superficial vs deep, size, metastasis, etc 3. Grade * Cell pleomorphism * Necrosis * Mitotic rate
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identify sarcoma type based on cell type. \*\*describe the cell type \*\*table 1. spindle cell (4) 2. small round (blue) cell (2) 3. Epitheliod cell 4. matrix producing 5. which sarcoma is biphasic \*\*what 2 cell types?
Table
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\*\*Identify sarco type based on General architectural patterns (table) 1. Fascicles of spindle cells 2. short fascicles of spindle cells radiating form center (storiform;pinwheel like) 3. Nuclei in columns (palisading) 4. Herringbone 5. which is biphasic (has spindle and epitheloid)
Table
84
identify 2 fatty tumors
1. Lipoma 2. Liposarcoma
85
Identify fatty tumor A. most common what? - soft or hard? mobile or immobile? painful?(exception?) B. common locations (2) C. what does the conventionaly histopathology look like? D. 4 variants; fibrous areas, small vessels, spindle cell areas, within muscle
**Lipoma** A. **MOST COMMON adult soft tissue tumor** * Soft, mobile * Painless with one exception (angiolipoma) B. Most common location: •Subcutaneous **trunk** and **proximal extremities** C. Conventional * Thinly encapsulated **yellow tumor** * **Lobules** of **mature fat** **D**. Other lipoma variants * Fibrolipoma: Fibrous areas * Angiolipoma: Small vessels * Spindle cell lipoma: Spindle cell areas * Intramuscular lipoma: Lipoma within muscle
86
Identify fatty tumor A, Adults 40-60 B. **Deep soft tissues** * Retroperitoneum (often very large) * Proximal extremities C. Types (4)
LIPOSARCOMA \*\*In retroperitonium 4 types * Well-differentiated (retroperitoneal) * Myxoid/Round cell (extremities) * Pleomorphic-**very aggressive** course * Dedifferentiated
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Most common type of **liposarcoma** **\*\***what mutation is amplified? \*\*what mutation is inhibited?
_Liposarcoma_, **Well differentiated** * Gross appearance same as lipoma * Micro can be very close to benign lipoma; Atypical spindle cells. Lipoblast: Cytoplasmic **vacuoles scallop nucleus** * Tend to be indolent with local recurrence * **MDM2 amplification** (inhibits p53)
88
Type of liposarcoma * **t(12;16)** FUS-DDIT3 fusion protein * Intramuscular, most often the thigh * **Round cell component is aggressive**; Rare lipoblast **Chicken wire pattern of thin capillaries**. Rare lipoblast
Liposarcoma, myxoid/round cell \*\*Chicken wire capillaries (thin vessels). Myxoid tend to be indolent
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Other types of liposarcoma (2) - very aggresive one - the other arise from well-differntiated liposarcoma
* **Pleomorphic** liposarcoma: Very aggressive * **Dedifferentiated** liposarcoma: Sarcoma arising from a well-differentiated liposarcoma
90
Types of **fibrous (myofibroblastic)** tumors/proliferations (4)
1. Benign reactive proliferations * Nodular Fasciitis * Myositis Ossificans 2. Fibromatoses * Deep fibromatosis (Desmoid) * Superficial Fibromatosis 3. Fibroma 4. Fibrosarcoma
91
identify type of fibrous tumor/proliferation **•MOST COMMON on volvar forearm** * Solitary rapidly growing 2-3 cm * May be painful * 10% history of trauma * Deep dermis, subcutis, or muscle * Reactive process, rarely recurs if excised * Spindle cell proliferation of fibroblasts
**Nodular fasciitis** \*\*Type of benign reactive proliferation
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Identify type of fibrous (myofibroblastic) tumor/proliferation * **Athletic adolescents and young adults** * 50% trauma * Subcutaneous and muscle * Early painful, circumscribed and firm * 3-6 cm * **Fibroblastic but later develops bone** * Ends as trabecular bone with marrow
**Myositis/Panniculitis Ossificans;** second type of benign reactive proliferation. \*\*The first is nodular fasccitis. \*\*Ossificans refer to bone
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Radiology: \*\*Identify tumor type? \*\*what is a differential that can be mistaken with this?
Myositis ossificans 3 weeks: Patchy flocculent radiodensities in the periphery Over time, radiodensity encroaches on radiolucent center Differential diagnosis: Extra-skeletal osteosarcoma of soft tissue
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2 types of fibromatoses
1. Superficial Fibromatosis * Palmer Fibromatosis * Plantar Fibromatosis (nodule on foot) * Penile Fibromatosis 2. Deep-seated Fibromatosis (Desmoid tumor) * Extra-abdominal * Abdominal * Intra-abdominal
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* Nodular or poorly defined fascicles of fibroblasts and abundant collagen * Course: May progress, regress or stabilize * May recur after excision
Superficial Fibromatosis
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identify fibrous tumor? (aka what disease) \*\*is it usually bilateral?
**Palmer Fibromatosis (Dupuytren’s contracture)** * Nodular thickening of palmer fascia; puckers skin and digit flexion contraction (mostly 4 and 5) * 50% bilateral
97
Identify fibrous tumor?
**Plantar fibromatosis (superficial firbromatoses)** * Bilateral infrequent * Irregular of nodular thickening of plantar fascia
98
identify tumor (aka what disease?) * Induration or mass on dorsolateral penis * Can cause abnormal curvature of penis * Can constrict urethra
* *Penile Fibromatosis** * *(Peyronie’s Disease**)
99
identify tumor group type * Large infiltrative; **Locally** **aggressive** and **Do not metastasize** * **Teens-thirties** * Mutations in **APC or β-catenin** * Recur if not completely excised; Wide margin needed
**Deep-seated Fibromatosis** (Desmoid Tumors) \*\*Type of fibrous tumor (4); _benign reactive proliferatin_ (nodular fisciitis, myosistis ossificans), _fibromatosis_ (superficial- palmar, plantar, penile and deep seated fibromatosis), _fibroma_, _fibrosarcoma_
100
identify fibrous tumor type * **Gray-white poorly demarcated** * Fibroblasts in fascicles infiltrate tissue \*\*\*Types
\*\*Types of **deep-seated fibromatosis** 1. Abdominal * Anterior abdominal wall * Women during or after pregnancy or C-section 2. Intra-abdominal Desmoid * Mesentery and pelvic walls * **Gardner Syndrome** 3. Extra-abdominal
101
Identify fibrous tumor - is it rare or common? what part of body? - 2 hallmark signs - spindle cell is in what pattern ? - how much recur? how much metastasize?
**Fibrosarcoma** * Rare; most common in **deep extremities** * Infiltrative fish-flesh with **hemorrhage and necrosis** * Spindle cell with areas of **herringbone pattern** * 50% recur; 25% metastasize
102
Types of skeletal muscle tumors - which is most common in kids (types?)
1. Rhabdomyoma (rare benign) 2. Cardiac rhabdomyoma (see chapter 12) 3. Rhabdomyosarcoma (most common in kids) * Embryonal * Alveolar * Pleomorphic
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\*\*Identify tumor? * **MOST COMMON Soft tissue sarcoma** of **childhood and adolescence**; rare after age 20 * Head/neck (nasal cavity, orbit, middle ear) * GU tract \*\*\*Specific components seen in cytoplasm (2)?
**Rhabdomyosarcoma** (skeletal muscle tumor) - **Desmin positive** (brown color in cytoplasm) - **MyoD1** (muscle transcription factor psitive) - same pattern for **myogenin**
104
identify tumor type * 60% of rhabdomyosarcomas * Children \< 10 years * Subtypes:?? in walls of hollow viscera and mucosal lined structures
**Embryonal Rhabdomyosarcoma** * Soft gray infiltrative mass * Mimic skeletal muscle embryogenesis * Round and spindle cells * **Sarcoma botryoides variant:** * “Cluster of grapes” protrude into lumen **•Cambium layer**: Submucosal hypercellular area •**Best prognosis amongst embryonal rhabdomyosarcoma**
105
106
Describe the slides \*\*components of what tumor type? myogenin markers positive or negative? Cross striations positive or negative? Round blue cells?
components of **embryonnal rhabdomyosarcoma** (in histopatho slide) - 3 1. **Rhabdomyoblast** (picture 2) * **Eccentric eosinophilic cytoplasm** with **thick and thin filaments** * Tadpole cells and strap cells * EM: Sarcomeres * **Myogenic markers positive: MYOD1, myogenin, desmin** 2 **Small round blue cells** (picture 1) 3. May see **cross striations** in some cells (picture 3 and 4)
107
Identify tumor type - tranlocation? - prognosis? - age range affected? - body part affected
Alveolar Rhabdomyosarcoma \*\*look like alveoli \*\*There are other variants **•Early to mid-adolescence** **•Deep muscles of extremities** •Fibrous septa divide tumor into alveolar-like spaces centrally containing discohesive cells while peripheral cells stick to wall **•t(2;13) or t(1;13)** **•PAX3 or PAX7 to FOXO1** fusion gene •**Poor prognosis** vs embryonal. \*\*Remeber that embryonal prognosis is good.
108
\*\*Identify skeletal muscle tumor type - age group? - mistaken for what othe rtumor type? - myogenn? desmin?
**Pleomorphic Rhabdomyosarcoma** * **Deep soft tissue** of **adults\*\*\* (**remember alveolar rhabdomyosarcome t2;13 is seen in early to mid adolescent) * Very pleomorphic with rhabdomyoblasts * Often **mistaken for undifferentiated pleomorphic sarcoma** * **Desmin positive** **•MyoD1 or myogenin positive**
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Prognosis of rhabdomyosarcoma
* Sarcoma botryoides: Best * Embryonal: Second best * Alveolar and Pleomorphic: Poor * 65% of children are cured * Adults do poorly
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•Benign smooth muscle tumor **•Most common in uterus (chapter 22)** Age group? \*\*\*\*\*other sites? - component of the slide? - rare in what body part
Leiomyoma * Skin: Erector pili, nipples, scrotum, labia; Pilar leiomyoma often painful and multiple. **Adolescent and early adults** * Bland smooth muscle cells in fascicles * Rare in deep tissues
111
Identify soft tissue tumor \*\*contents ? what is present vs absent? (myogenin? myoD1, actin? desmin?)
**Leiomyosarcoma** * 10-20% of soft tissue sarcomas * F \> M * Skin, deep extremities and retroperitoneum * White masses can be large * _Malignant spindle cells_ **•Smooth muscle actin and desmin** •**Negative** for _MyoD1 and myogenin_
112
\*\*identify soft tissue tumor - tranlocation and fusin gene - cell type \*\*\*what is UNIQUE about this? - Classic location?\*\*\*
**Synovial Sarcoma** * Originally believed to recapitulate synovium but cell of origin is unknown: \<10% intra-articular * 10% of soft tissue sarcomas * Age 20-40s * Deep and around large joints - **classic is around knee** * 60-70% lower extremities, especially knee/thigh * Often microcalcifications on X-ray * **t(X;18) SYT-SSX1 or SYT-SSX2 fusion** * Prognosis: 25-60% 5 yr **\*\*\*ONLY BIPHASIC TUMOR**
113
2 types/variants of synovial sarcoma \*\*Do they both stain positive for cytokeratins?
1. **Biphasic** (dual) differentiation: * Epithelial cells as glands, cords, or nests * Spindle cells: cellular in fascicles 2. **Monophasic** (spindle cell) variant •Positive for cytokeratins (epithelial marker), epithelial membrane antigen (EMA) \*\***Yes both stain positive for cytokeratins - only tumor that does this (Synovial sarcoma)**
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* **Group of aggressive neoplasms** * Diagnosis of exclusion * Proximal extremities and retroperitoneum * **Large grey, hemorrhagic and/or necrotic** * Metastasis 30-50% \*\*Identify cell pattern
Undifferentiated Pleomorphic Sarcoma (**Malignant Fibrous Histiocytoma**) •\*\*Cell **pleomorphism and storiform pattern**
115
Immunohistochemistry of soft tissue tumors - which is specific for skeletal muscle? - smooth muscle? - non epithilial tumor?
* Epithelial membrane antigen and cytokeratin: General epithelial marker * MyoD1 and Myogenin: Skeletal muscle * Actin and desmin: Skeletal or smooth muscle * Vimentin: Nonepithelial tumors * **Smooth muscle actin: Smooth muscle** **•Epithelium: Cytokeratin and EMA** **•Skeletal muscle: MyoD1, Myogenin, Desmin and Actin** **•Smooth muscle: Desmin and Actin** **•Nonepithelial tumors: Vimentin**
116
Summary list of soft tissue tumors **Spindle cells**; give examples of beign and malignant tumors in the following - myofibroblastic - smooth muscle - unknown
117
Summary list of soft tissue tumors Small round blue cells; give examples of beign and malignant tumors in the following - skeletal muscle - fat - lymphocytes
118
What soft tissue tumor is biphasic ?? \*\*is it benign or malignant?
SYNOVIAL SARCOMA \*\*malignant
119
Identify painful skin lesions "Blue ANGEL" (6)
* BLUE rubber bleb nevus * Angiolipoma * Neuroma (traumatic) * Glomus tumor * Eccrine spiradenoma * Leiomyoma (cutaneous)
120
1. What is the most common form of arthritis? 2. What is the most common bacteria in septic arthritis in teenagers? 3. Where are the osteophytes located in the hand in rheumatoid arthritis?
1. What is the most common form of arthritis? **Osteoarthritis** 2. What is the most common bacteria in septic arthritis in teenagers? **Gonorrhea** 3. Where are the osteophytes located in the hand in rheumatoid arthritis? **MCP**
121
identify condition * Progressive, irreversible condition involving loss of articular cartilage, causing pain and deformity * Involves weight bearing joints mainly. * Associated with Age, Obesity, and hx of trauma * Mechanical Wear and Tear * Histological changes not only associated with age. \*\*Identify symptoms, exam findings, x-rays
**Osteoarthritis** •**Symptoms** –Stiffness, pain, deformity –Worse at end of day, in the groin for hip OA •**Exam** –_Heberden’s nodes at DIP and Bouchard’s nodes (PIP) in hand_ –Painful, decreased ROM •**X-rays** –Loss of joint space –Sclerosis –Subchondral cysts –Osteophytes
122
treatment options for osteoarthritis (10)
–Weight loss –PT (better biomechanical function of joint) –Bracing –Glucosamine / Chondroitin? –NSAIDS –Cymbalta? (helps with depression) –Steroid Injection (last 3 months) –Viscosupplementation (inject stuff that will produce protein synovial fluid in mild-moderate degenerative changes) –**Arthroscopic debridement** (_successful in **wrist and elbow**_ but not helpful in knee arthritis. Hip not studied) –**Joint Replacemen**t (_most successful in **hip and knee**_ and shoulder). Risk for dislocation, infection, stiffness. Longevity 10-20 years.
123
identify condition * Systemic Autoimmune Disorder with inflammatory synovitis that destroys cartilage * F \> M, 50s * Symmetrical distribution of joints; both sides \*\*Patient must present with 4 of what 6 symptoms \*\*Other symptoms
Rheumatoid Arthritis •**Four of the following** –Morning Stiffness 1 hour –Arthritis of 3+ joints for 6 weeks –Systemic arthritis for 6 weeks –Rheumatoid nodules –+ RF factor (80%); **POSITIVE RHEUMATOID FACTOR** –Radiographic changes •Malaise, fatigue, tenosynovitis, CTS, vasculitis, keratoconjunctivitis sicca, pulmonary nodules, inflammatory pericarditis.
124
Exam, tests and X-rays of rheumatoid arthritis
•Exam –Joint contractures, effusions, deformity –Ulnar deviation of the hands –PIP and MCP nodules and inflammation –Bogginess of the joints •Tests –RF (IgM antibodies against the Fc portion of IgG) HLA-DR4 –ESR and CRP elevated (because it is an inflammatory arthritis) •X-rays –Bony erosion, joint space loss –C1-2 instability! (common place to develop instability)
125
Treatment options for rheumatoid arthritis
•Treatment –NSAIDs –Steroids –DMARDs; Hydroxychloroquine, methotrexate, gold, **Embrel** –Surgery
126
identify condition * Infection in the Joint * Most common in kids from hematogenous spread * Adults are often immuno-compromised * **Metallproteases** cause permanent destruction in about 8-12 hours (lead to loss of articular cartilage) \*\*Identify symptoms, exam and labs
**Septic arthritis** •Symptoms –Acute illness, fever, tachycardia –**PAIN WITH ROM OF JOINT** •Exam –Look for source –Slight flex to joint –**Passive ROM is very painful** •Labs –Elevated or normal WBC –Elevated ESR, CRP –Blood Culture –Xrays normal in acute setting –**Joint Aspirate = \>50000 WBC / mm3**
127
Identify common bugs that cause septic arthritis in the following 1. neonate 2. \<5y.o 3. \>5y.o to

4. adolescents

5. adults

6. Sickle cell patients

7. Chronic picture

**What is most classic bug in sickle cell? most common bug in sickle cell? most common bug in adolescents of sexually active people?

–Neonate = Staph Aureus, Group B Strep –\<5yo = Staph Aureus, group A strep, H flu, strep pneun –\>5 to

–Adolescents = Gonorrheoeae

–Adults = Staph Aureus

–Sickle Cell Patients = Salmonella

–Chronic Picture = TB or Lyme

**

-In sickle cell patients, most classic bug is SALMONELLA. The most common bug is STAPH AUREUS

-In sexually active patients esp adolescents, most common bug is GONORRHEA

128
treatment for septic arthritis (2)
–Surgical washout –Antibiotics
129
4 types of seronegative spondyloarthropathies
1. Ankylosing spondylitis 2. Reiter disease 3. Psoriatic arthritis 4. IBD
130
Identify type of seronegative spondyloarthropathy - ankylosing spondylitis - frequency? - what happens to joints? - 2 charateristic features (labs) - 3 presentations/conditions
•Ankylosing Spondylitis –1 in 2000 persons (most common) –SI joints, spine, Stiff Joints –HLA-B27 +, RF – –Uveitis, carditis, enthesitis (inflammation of attachment points for many tendons)
131
identify type of seronegative spondyloarthropathy –After Urethritis, cervicitis, or dysentery –Reactive arthritis 2-8 weeks after infection –Enthesitis, dactilitis, sacroiliitis, conjunctivitis –Chronic recurrent arthritis
REITER DISEASE
132
Identify types of seronegative spondyloarthropathy –Nail disorders –Iritis
Psoriatic arthritis –5-10% of those with psoriasis
133
identify type of seronegative spondyloarthropathy –10-20% of those with IBD, more in Crohns –HLA-B27 in 50-70% –Sacroiliitis, spondylitis, and arthritis of the knee and ankle
IBD (inflammatory bowel disease)
134
Seronegative spondyloarthropathy - symptoms - exam - labs - treatment
**•Symptoms** –Back pain –Morning stiffness •**Exam** –FABER (flexion, abduction, external rotation) tests SI joint –Enthesitis (where tends attach) **•Labs** –HLA-B27 –Xrays of spine (stiff and painful spine) •**Treatment** –NSAIDS, MTX –Surgery
135
136
1. For osteoarthritis, is the pain worse at the beginning or end of the day? 2. What is the incidence of Ankylosing Spondylitis? 3. Rheumatoid arthritis patients that undergo surgery must have what part to their spine evaluated to prevent cord injury?
1. End of day 2. 1 in 2000 persons 3. C1-2 instability
137
1. What are the five most common primary carcinomas that metastasize to bone? 2. What is the most common bacteria that causes osteomyelitis? 3. What is the difference between the T and Z score in the DEXA Scan?
1. 5 most common primary carcinoma that mets to bone? (PT Barney Likes kids) - **Prostate, Thyroid, Breast, Lung, Kidney/renal cancer.** 2. What is the most common bacteria that causes osteomyelitis? **Staph aureus** 3. What is the difference between the T and Z score in the DEXA Scan? **_T score_ compared to _25yo female_, _Z score_ compared to _age matched peer_.**
138
MSK tumors - tumors come from where? - cancers called? frequency? - metastasize to what organ?
MSK tumors * Tumors come from the **mesodermal tissue** (connective tissue like bone, fat, muscles) * Cancers are called “sarcomas” and are **very rare** (only 15000 in US each year, vs 250000 Breast cancers every year.) * They like to **metastasize to the lung**
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MSK tumors (4 types) 1. Non-ossifying Fibroma, Enchondroma, Unicameral Bone Cyst, Fibrous dysplasia, Eosinophilic Granuloma, Aneurismal Bone Cyst, Giant Cell Tumor of Bone 2. Metastatic disease, Osteosarcoma, Ewing’s Sarcoma, Chondrosarcoma, Multiple Myeloma 3. Ganglion, Lipomas, Arterio-Venous Malformation, Giant Cell Tumor of tendon sheath 4. Malignant Fibrous Histiocytoma, Liposarcoma, Leiomyosarcoma, Rhabdomyosarcoma
1. **Benign Bone:** –Non-ossifying Fibroma, Enchondroma, Unicameral Bone Cyst, Fibrous dysplasia, Eosinophilic Granuloma, Aneurismal Bone Cyst, Giant Cell Tumor of Bone 2. **Malignant Bone:** –Metastatic disease, Osteosarcoma, Ewing’s Sarcoma, Chondrosarcoma, Multiple Myeloma 3. **Benign Soft Tissue:** –Ganglion, Lipomas, Arterio-Venous Malformation, Giant Cell Tumor of tendon sheath 4. **Malignant Soft Tissue:** –Malignant Fibrous Histiocytoma, Liposarcoma, Leiomyosarcoma, Rhabdomyosarcoma
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MSK tumors 1. History (4) 2. Physical exam (4)
**1. History** –Age (**osteosarcoma 1st decase, ewing/PNET in 2nd decade, chondrosarcoma later in life in 50s, metastatic disease - over 40 years of age**) –Mass formation (**may not be rapidly growing**) –Pain (**night achy pain** in bone tumors, painless in soft tissue) –History of **Prostate, Lung, Breast, Thyroid, or Renal Ca?** •Most common carcinomas that met to bone **2. Physical Exam** –Mass –Tenderness? –Joint swelling? –Limp
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MSK tumors What can be found from the following tests - xray of limb - bone scan - MRI - CT chest/abdomen/pelvis - CBC diff, CMP - ESR/CRP - SPEP/UPEP - TSH/Thyroid US - UA - PSA - Mammogram - CXR
–X-rays of the limb: Bony destruction –Bone Scan: Bony activity, skip lesions –MRI: Assess soft tissue anatomy –CT Chest / Abdomen / Pelvis: Look for primary or mets to lung –CBC diff, CMP: Anemia, Alk Phos –ESR / CRP: Infection? –SPEP / UPEP: Myeloma? –TSH / Thyroid US: Thyroid? –UA: Renal? –PSA: Prostate? –Mammogram Breast? –CXR: Lung? –
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MSK tumors 1. - what happens over age 40? - growing soft tissue masses are? 2. treatment of MSK tumors
1. * Over age 40, bone tumors are most likely **metastatic** * Growing soft tissue masses are most likely malignant 2. **Treatment:** –Benign Soft tissue \>5cm or deep recommend excision –Malignant Soft tissue recommend resection, chemo?, radiation? –Benign Bone recommend excision if **aggressive** –Malignant Bone recommend chemo, resection, reconstruction, radiation? (not first line treatment)
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Identify treatment of MSK tumors 1. Ewing/PNET 2. Osteosarcoma 3. Chondrosarcoma
1. **Ewing** – rad onc, surgery, chemo (MTX, vincristine, cyclophosphamine. 2. **Osteosarcoma** – no radiation, **Neoadjuvant chemo (doxorubicin - cardiotoxicity, cisplatin, MTX),** wide resection, reconstruction and chemo. 3. **Chondrosarcoma** – surgery, Osteomyelitis – Abx, ID)
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MSK tumors - age and histopath 1. Ostosarcoma 2. Ewings/PNET 3. Chondrosarcoma 4. metastatic disease
**Osteosarcoma**; 1st decade, swelling and night pain, **HIstopatho – Pink plus osteoblasts** (thick osteosarcoma) with football shaped cell. **Ewings/PNET**; 2nd decade of life. Swelling and night pain. Translocation 1 (11,22). diaphyseal to metaphyseal **Chondrosarcoma**; later in life in age 50s. **tooth achy pain**. _Histopath – bluish purple_ (sheets of marble) – pleomorphic. Treatment – cut it out **Metastatic disease**; over age of 40. Look like carcinoma
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Identify condition - Osteomyelitis 1. what happens to bone? what part of bone is preferred? 2. Most common bacteria? 3. How is it spread?
1. Infection of the BONE itself –Prefers the **metaphysis** (area from growth plate to center of bone) 2. Most common bacteria is **Staph Aureus**, followed by **hemolytic strep.** –TB, syphillis, fungus and virus too. 3. Most commonly **spread hematogenously**, but can be introduced through direct innoculation with open fractures.
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History and exam of osteomyelitis \*\*do you have pain with ROM ?? (as opposed to what joint condition?)
•History: –Achy, unrelenting night pain –Fever •Exam: –Tenderness in bone –ROM of joints is ok; Unlike in septic arthritis –Swelling, warmth, redness, draining sinus
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Osteomyelitis - tests \*\*What is the gold standard for diagnosis \*\*Identify other tests and why order them (5)
–CBC with Diff: Elevated WBC with left shift –ESR / CRP: Elevated inflammatory markers –X-rays of limb: May show **Brodie’s** abscess –Blood Cx: May grow bug from hematogenous spread **–_Bone Cx_: Gold standard for diagnosis** –MRI / BS: Very helpful to assess abscess and extent
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Treatment of osteomyelitis
•Treatment: –Empiric treatment with ABX (Vanc) while waiting for Cx –Surgical washout if no improvement in 2 days, or if there is a clear abscess –If chronic (eg diabetics), may need multiple treatments
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Identify condition •Low bone mass leading to microarchitectural deteriorization, causing increase fragility of bone –Hip, Spine, Wrist, Shoulder Fractures. –25% mortality rate at 1 year for all hip fractures! •10 mil+ persons, 1.5 million fractures per year, $18billion in costs.
Osteoporosis
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2 types/forms of osteoporosis - which has type I and II (describe them)
**•Primary** –Type I, postmenopausal osteoporosis, caused by hormonal changes leading to bone loss –Type II, senile osteoporosis, caused by altered calcium metabolism leading to bone loss **•Secondary** –Due to long term steroid use, hyperparathyroidism, hyperthyroidism, renal failure, cancers, metabolic abnormalities, connective tissue diseases, long term immobilization
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History and exam of osteoporosis
•History –Over 65 –Postmenopausal –Family history –Personal history of low energy fracture –Smoker –Low BMI (skinny) –Steroid use **•Exam** –Loss of height –**Thoracic kyphosis** (hunchback) –Loss of menstruation
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What tests to detect osteoporsis and why order them
•Tests: –**DEXA Scan** of spine, hip, or femur * T score is compared to 25yo female * Z score is compared to age matched peer * **\< -2.5 SD below mean is osteoporosis** –**NTx**: Measures bone collagen (NTx should decrease in urine once you start treatment) –**CBC**: Anemia = Multiple Myeloma? –**ESR / CRP**; Infection? –**TSH / PTH**; Hyperthyroid / HyperPTHism –**SPEP / UPEP** ; Multiple Myeloma –**Ca / P / Alk Phos / Vit D** ; Osteomalacia –**BUN / Cr / LFT**; Renal / Liver causes
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identify prevention and treatment of osteoporsis
**•Prevention:** –Maximize Ca / Vit D, and WB exercise (Esp \<30) –Minimize smoking, caffeine, meds **•Treatment:** –Bisphosphonates; (works by disrupting ruffled border of osteoclasts) –Calcitonin –Pulsed PTH –SERMS (not recommended)
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* What is the most common metastatic site for sarcomas? * Why does osteomyelitis most commonly happen in the metaphysis of the bone? * Name one common medicine that with long term use can cause secondary osteoporosis.
* What is the most common metastatic site for sarcomas? **Lung** * Why does osteomyelitis most commonly happen in the metaphysis of the bone? **Turbulent flow here. Metaphyseal blood flow allows for watershed area for bacteria to pool** * Name one common medicine that with long term use can cause secondary osteoporosis. **Steroid**
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* 1. What is the most sensitive physical exam test to assess patency of the ACL? * 2. What muscle is involved in tennis elbow? – * 3. What systemic disease is often associated with olecranon bursitis? * 4. What condition is associated with “Popeye arm”?
* 1. What is the most sensitive physical exam test to assess patency of the ACL? **Positive Lachman’s test (25 degrees)** * 2. What muscle is involved in tennis elbow? – **on lateral epicondylitis – ECRB (extensor carpi radialis brevis muscle)** * 3. What systemic disease is often associated with olecranon bursitis? **Gout** * 4. What condition is associated with “Popeye arm”? **Rupture of long head of biceps, with labral injury**
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1. what is the primary stabilizer of the knee? what does this prevent? 2. If this tears, what are the symtoms? 3. What do you check for in exam? (3) 4 tests (2); one will be negatuve the other will be positive 5. treatment (2)
**ACL TEAR** 1. **ACL** is primary stabilizer of knee, preventing anterior tibial translation. 2. Symptoms * Popping sound, hemarthrosis, knee instability * Associated with meniscal tear 50% 3. Exam * Effusion (from hemarthrosis) * Positive Lachman’s, Positive Anterior drawer (50%) 4. Tests * Xrays negative (ant translation of tibia?) * MRI positive 5. Treatment * PT (hamstring strength) * ACL reconstruction for unstable knees (in athletes)
157
Identify condition in sports - **idiopathic loss of shoulder motion** **-** associated with what systemic disease? - symptoms (2) - exam (2) - tests - treatemnt
**Frozen Shoulder;** Idiopathic loss of shoulder motion, **associated with Diabetes,** 40-60yo. 1. Symptoms * Early freezing, then thawing over 6-24 months * Pain may be associated with this 2. Exam •Loss of 50% of active and passive ROM **•Painful deltoid insertion** 3. Tests •Xray are negative 4. Treatment (**mainly symptomatic**) * NSAIDs, Injections, ROM with PT * Arthroscopic lysis of adhesions and **_MUA?_**
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Identify sports condition - **Inflammation of subacromial bursa and rotator cuff tendons in middle aged persons** - symptoms - exam - tests - treatment
Impingement Syndrome; **Inflammation of subacromial bursa and rotator cuff tendons in middle aged persons** 1. Symptoms •Lateral shoulder pain with overhead activity 2. Exam •Positive Hawkins, Supraspinatous tests. No weakness. Just pain 3. Tests * Xrays negative * MRI shows inflammation but no tear 4. Treatment * PT * **Steroid injection** - Surgical decompression
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Identify sports condition •Degenerative painful condition of the ECRB (lateral) tendon and / or flexor-pronators (medial) - symptoms - exam tests treatment
**Elbow epiconylitis** * **Degenerative painful condition of the ECRB tendon and / or flexor-pronators.** * Symptoms * 35-50 yo with pain on either the medial or lateral epicondyle with activity * Exam * Pain with resisted extension of the wrist with forearm pronated (lateral) * Pain with resisted flexion of the wrist with forearm pronated (medial) * Tests * Xrays negative * Treatment **•Tennis elbow strap**, ice, larger grips, PT, NSAIDS * Steroid injection * Surgical debridement (stimulate inflammatory response that cause healing) * BS * Anatomy of elbow, mechanism of NSAIDS and Steroids
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Identify sports condition \*\*Indicate test and treatment (what is **diagnostic?**) * Symptoms * **Locking and catching in the knee** * Exam **•McMurrays +** •Joint line tenderness
Menisci tear; **Fraying or tear of menisci** * Tests * Xrays negative * **MRI shows tear – diagnostic** * Treatment * PT * Arthroscopic debridement * BS * Anatomy of knee
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Identify sports condition \*\*What systemic condition is associated with this? •Symptoms **•Swelling, painful posterior elbow** * Exam * Mass over tip of elbow, tender, red, hot * Tests * Aspiration for crystals and infection * Treatment * NSAIDS for acute, ice * Surgical removal * BS * Anatomy of elbow. Mechanism of NSAIDS, Micro for infection
**Olecranon Bursitis** - inflammation of olecranon bursa \*\*associated with **Gout**
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Identify sprots conditon * Symptoms * Achy pain anterior knee worse after long periods of sitting, and climbing stairs * Exam * Q angle (anything greater than 15 in females and 10 in males) * Patellar apprehension * Resisted extension of knee * Tests * Xrays normal * Treatment * PT for quad strength
**Patellofemoral pain** - Pain around the patella without signs of arthritis, common in teenagers during growth spurt
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identify sports condition * Symptoms * **Worse heel pain in AM (morning) insidious onset** * Exam * Tender on medial and lateral calcaneous, tight dorsiflexion * Tests * Xrays show heel spur, which is NOT cause of pain, but symptom. * Treatment * NSAIDs, heel cups, stretches of heel cord * Injections * Surgical release * BS * Anatomy of foot, Histology of tendonosis
**Plantar Fasciitis** - **Degenerative** tear of plantar fascia, **more common in women and overweight persons** with tight gastroc-soleus tendons
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Identify sports condition * Symptoms * Pain with overhead activity, catching, grating sensation * Exam * **Positive Drop arm**, Hawkins, weak supraspinatous, weak external rotation * Tests * Xrays may show high riding humeral head * MRI shows discontinuity of tendon * Treatment * PT, NSAIDS * Repair of tendons (Arthroscopically or open)
**Rotator cuff tear** - Tear of supraspinatous (most common), infraspinatous, subscapularis, or teres minor. •Acutely in young, chronic degeneration in older.
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identify * Symptoms * Sudden pain, bulge in arm * Exam * **Popeye arm, pain with supination (biceps major supinator of forearm)** * Tests * Xrays negative * MRI shows tear with hematoma * Treatment * NSAIDs, PT Occasionally will tenodesis.
**Rupture of proximal biceps tendon;** •Rupture of long head of biceps, with labral injury
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* Symptoms * Lateral hip pain, unable to lie on side. * Exam * Point tender over posterior GT * Ober’s test * Tests * Xrays negative * MRI shows swelling of bursa * Treatment * NSAIDs * PT for stretches and strengthening
**Trochanteric bursitis** - Inflammation of greater trochanteric bursa from tight IT band
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* 1. What systemic disease is associated with Frozen Shoulder? * 2. Is the Drop Arm Test positive in patients with Impingement syndrome? * 3. Are heel spurs the cause of the pain in planter fasciitis? * 4. Where is the pain for trochanteric bursitis?
* 1. What systemic disease is associated with Frozen Shoulder? **Diabetes** * 2. Is the Drop Arm Test positive in patients with Impingement syndrome? **Positive positive hawkins and supraspinatous test?? You see positive drop arm test in rotator cuff tear** * 3. Are heel spurs the cause of the pain in planter fasciitis? **No it is not the cause of pain – it is just a symptom** * 4. Where is the pain for trochanteric bursitis? **Lateral hip pain, unable to lie on side**
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1. 3 bones that attach to knee 2. suppoting stuctues of the knee
1. Femur, tibia, fibula 2. capsule, ligaments, minisci, muscle
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identify condition of the knee - restricts anterior translation of tibia - restricts rotational motion - 50-70% hear a pop, knee swelling after (hemarthrosis) - LACHMAN TEST IS POSITIVE; flex knee to 30 degrees - stabilize femur with one hand and use opposite hand to apply anteriro directed force to posterior tibia \*\*Identify indicence, which gender has higher risk treatment?
ACL - Anterior cruciate ligament - very common, increasing incidence - very good surgical results - More commonly **non-contact** injury with plant-and-pivot or stop-and-jump mechanism (abrupt decelaration, landing on a flat foot with knee in extension and valgus) - women have higher risk with similar exposure Treatment; 1) Non-op treatment 2) Bracing 3) Operative ACL construction - for atheles and more active poeple 4) BTB autografts
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identify types of graft used to reconstruct ACL
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Advantages and diasvantages of BTB autograft used in ACL reconstruction
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identify condition Mechanism of injury; twisting on a flexed knee and deep squatting S&S; effusion, tender along joint like, cathcing, locking and decreased ROM \*\*what is the main test performed? \*\*what does treatment depend on?
**Meniscus tear** \*\***MucMurrys**; clicking or pain indicate positive test \*\*Decision to **repair or resect depend on the blood supply**. in young active person, try to repair the meniscus and give it a chance to heal. You don't want to resect (remove) in yound person.
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identify condition - mostly anterior dislocation (basketballer) - GH joint has largest ROM in body - poor articular conformity
**ANTERIOR SHOULDER DISLOCATION**
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Identify body part \*\***Loss reduces force to dislocate 50%** - triangular rim of fibrocartilaginuous tissue; extension of bony glenoid.
LABRUM Attachment sites; GH ligaments, capsule, biceps
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Epidemiology of labrum tear (lead to anterior shoulder dislocation) - age with higher probability of another dislocation (based on age)
- probability 50% of re-dislocation in **men at 27 years** and **women at 17 years old**. \*\*Arthroscopic labral repair - helps
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Identify - most common sports-related injury (up to 50% of all sports injuries); basketball injuries and even pro golfers - NOT A BENIGN INJURY -
**"Low" Ankle Sprain**
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Tests of lateral ankle sprain exam (2)
1. Anterior drawer 2. Tala tilt
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Grades/severity of ankle sprain (injury, swelling, weight bearing)
Grade 1; ATFL strecth Grade 2; ATFL and capsular tear + CFL Grade 3; AFTL, capsule, CFL tears \*\*Do not ignore it - benign neglect can lead to high recurrence rates
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How to treat ankle sprain (3) \*\*another one does not treat but prevent recurrence \*\*when do you need surgery
1. RICE 2. Protect ligaments 3. Functional rehabilitation (early joint mobilizaion); help prevent recurrence 4. Taping/Brace shown to prevent recurrence of ankle sprian \*\*\*Surgery indicated when functional rehab has failed and pt has chronic pain and instability symptoms
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Skeletal muscle - definition a. muscle pathology b. inherited disorder c. destroy part of myocyte or muscle cell d. muscle regenerate from satellite cels e. response to increased load
a. Myopathy: Disorder of muscle b. Muscular Dystrophy: * Inherited disorder * Progressive muscle weakness and wasting c. Segmental Muscle Necrosis: Destruction of a portion of the myocyte length d. Muscle regeneration: Satellite cells reconstitute destroyed muscle e. Fiber hypertrophy: Response to ↑ load
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Skeletal muscle - definitions - tonic spasms - deficeint ton e - fixation joints - high enzyme in muscle and brain
* Myotonia: Tonic spasm of one or more muscles; also a condition characterized by such spasms * Hypotonia: Deficient tone or tension * Arthrogryposis: Fixation joints in an extended or flexed position * Creatine (phospho)kinase (CK;CPK): Enzyme highly concentrated in muscle and brain
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\*\*\*\*\*Identify sign - skeletal muscle * indicates weakness of the proximal muscles * Uses the hands and arms to "walk" up from a squatting position
**GOWER'S SIGN**
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\*\*Picture of I and A band - which is light vs dark band - During contraction; which shortens and which remains unchanged?
Picture **Contraction**: I band shortens (LIGHT COLOR); A band is unchanged (DARK COLOR)
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Differences in type 1 vs type 2 based on fiber type - action type - actin - fibers (slow or fast) - metabolism
Picture
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Muslce fibers - type 1 summary? - what determines muscle types \*\*\*describe the following; color of type 1 in normal ATPase (9.4), fiber type grouping, grouped atrophy
* “**One (1) slow fat (lipid rich) red (high myoglobin) ox (oxidative)”** * **Innervating motor neuron** determines muscle type **•Fiber type grouping**: Neuron/axon drop out leads to larger motor units (muscle fibers per neuron) •**Grouped atrophy**: Loss of a motor neuron leads to atrophy of associated muscle
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Identify condition * Disorder of motor neurons * Breakdown of myosin and actin * Resorption of myofibrils
Denervation Atrophy
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Idnetify skeletal condition * Progressive **destruction of anterior horn cells and cranial nerve motor neurons** * Type 1: 0-4 months onset with severe hypotonia * Type 2: 3 months – 2 yrs onset * Type 3: \> 2 years onset; can survive to adult * Autosomal recessive **•Survival Motor Neuron 1 (SMN1)**
Spinal Muscular Atrophy (Infantile Motor Neuron Disease; SMA)
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Identify skeletal condition * Inherited disorders * Often begin in childhood * Progressive muscle weakness and wasting * May affect heart * Pathology: * Variation in fiber size * Internal nuclei * Degeneration, necrosis, phagocytosis of fibers * Later replaced by fibrofatty tissue
Muscular Dystrophy \*\*Most common type is DMD
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Identify skeletal condition * Dystrophin protein defect from abnormal gene at Xp21 (deletion \> frame shift or point mutation) * Huge gene (2.3 x 106 base pairs) * X-linked * Most common type of MD: 1/3500 male births * Manifest before 5 and in wheel chair by 12 * Death in 20s * 2/3 familial; 1/3 new mutations
DMD
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* Normal at birth * Delayed walking then clumsy * Weak pelvic then shoulder girdle * Pseudohypertrophy of calves as fibers ↑ size * ↑ CK; later returns to normal with muscle loss * Impaired cognition * Death: Respiratory failure, cardiac decompenstation, or lung infection * Female carriers may have ↑ CK; risk for cardiomyopathy
DMD
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identify condition
DMD- Duchenne Muscular Dsytrophy
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Identify skeletal condition * Defect in Dystrophin quality/quantity of protein from abnormal gene at Xp21 * Less common than DMD * Less severe than DMD * Later onset than DMD
Becker MD
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MD female carrier DMD vs BMD - dilated cardiomyopathy - LV dilation by echo - elevated CK - Weakness
Picture \*\*In BMD, no chance of dilated cardiomyopathy
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Skeletal muscle condition * **Proximal muscles affected** * AD, AR * Begin to walk with a “waddling” gait because of weak hip and leg muscles. **•Trouble getting out of chairs or climbing stairs** **•Weakness in the shoulder** make reaching over the head, holding arms outstretched or carrying heavy objects difficult. •Many related to **dystrophyn glycoprotein complex**
**Limb Girdle** Muscular Dystrophy
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identify skeletal condition * **Facial weakness** * Wasting of the upper arm and shoulder muscles. * The scapular bones look like wings when the arms are raised **\*\*\*WINGED SCAPULA**
Facioscapulohumeral MD
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identify skeletal condition •Onset 10-20; Triad 1. Early on humeroperoneal weakness (proximal in the upper limbs and distal in the lower limbs) 2. Prominent contractures, especially elbows and ankles **3.Cardiomyopathy**
Emery-Dreifuss MD
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skeletal condition **A. Myotonia (sustained involuntary contraction)** * Stiffness * Difficulty releasing grip * Can be elicited by percussion of thenar eminence * http://www.youtube.com/watch?v=KuhW4F4OhIA **B. Onset in childhood** **C. Other muscle features:** * Abnormal gait from weak foot dorsiflexion * Weakness of intrinsic hand & wrist extension **_•Facial muscle atrophy and ptosis_**
**Myotonic dystrophy**
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Skeletal condition * Other clinical findings * Cataracts * Endocrinopathy * Cardiomyopathy * **Autosomal Dominant** **•Dystrophila myotonia-protein kinase (DMPK)** * CTG repeat expansion on 19q * Normal \< 30 repeats; MyD has thousands * Number of repeats expands with generations **•Anticipation: Onset at a younger age in succeeding generations**
**Myotonic Dystrophy** \*\*\*Many **CTG repeats** expansion on 19q \*\*Anticipation \*\*Characteristic face - **drooping, gaping mouth**, arthrophy, **_myotonia_**, **christmass tree cataract**
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identify skeletal condition * Familial * Myotonia and/or hypotonic paralysis * Malignant hyperpyrexia
**Ion Channel myopathy** ; Channelopathies” mutations in ion channels \*\*Most common is **hypokalemic periodic paralysis**
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Types of hypotonic channelopathies (3)
**1. Hypokalemic Periodic Paralysis** * Most common 1/100,000 * Ca++ channel mutations most common * Onset: First-second decade * Attacks of flaccid weakness provoked by * Carbohydrate-rich meal, exercise, heat, cold, stress, medications **2. Hyperkalemic Periodic Paralysis** **3. Normokalemic Periodic Paralysis**
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identify channelopathy - complication from surgery (from anesthesia) - very high fever, tachypnea, muscles completely contrat (over heating will then happen)
**Malignant Hyperthermia/Hyperpyrexia** - Many identified genes: * Ca++ channel * Ryanodine receptor RyR1 (RYR1 gene) - Sudden hypermetabolic state with tachypnea and general muscle contration - Triggered by anesthesia: Halogen containing gases or succinylcholine \*\*treated by Dantrolene
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Identify condition * Release Ca++ from sarcoplasmic reticulum * ATP is depleted by muscle contraction * Anaerobic metabolism: Lactic acidosis * Hyperthermia * Rhabdomyolysis * Hyperkalemia * Renal failure **•Treatment: Dantrolene**
Malignant Hyperthermia/Hyperpyrexia
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skeletal condition * Defined by pathologic findings on biopsy * Onset early in life * Nonprogressive or slowly progressive * Proximal or generalized weakness * May present as * Hypotonia (“floppy baby”) Arthrogryposis congenital fixation of a joint in an extended or flexed position
Congenital Myopathy
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* Autosomal dominant * Hypotonia * Ryanodine receptor -1 (RYR1) gene defect * Risk for malignant hyperthermia * Centrally light area in type 1 fibers
Central core disease
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Various types: Autosomal dominant and Autosomal recessive * Nonprogressive hypotonia, weakness * Delayed development in kids * Involves proximal limb muscle * Subsarcolemmal spindle-shaped particles from Z-band (α-actin) material
Nemaline myopathy
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A. Various types (3) * X-linked * Autosomal dominant * Autosomal recessive: B. Central nuclei usually confined to type 1 fibers
Centronuclear (myotubular) Myopathy
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* Accumulate lipid in myocytes * Defects in carnitine transport system * Defects in mitochondrial dehydrogenase enzyme system
Lipid myopathy
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* Oxidative phosphorylation diseases” * Defect may be mtDNA or nuclear DNA * Many manifestations * Can present as young adult * Ragged red fibers from aggregated mitochondria * Mitochondria “parking lot” paracrystalline inclusions
Mitochondrial myopathy \*\*Kmart
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Identify picture \*\*\*RED RAG FIBERS
Mitochondrial myopathy (Kmart - red ragged fibers) Mitochondrial myopathy is a rare disease marked by the appearance of "ragged red fibers" containing aggregates of abnormal mitochondria that appear subsarcolemmally and and scattered through some muscle fibers. They appear on H&E staining here as granular red areas. This disorder results from abnormal synthesis of mitochondrial proteins directed by mitochondrial DNA. Thus, inheritance is maternal.
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Inflammatory myopathies 1. infectious e.g 2. Noninfectious (3) 3. systemic inflammatory disease (2)
**1. Infectious** •Trichinella spiralis **2. Noninfectious** * Dermatomyositis * Polymyositis * Inclusion Body Myositis **3. Systemic Inflammatory Diseases** * Systemic Sclerosis (Scleroderma) * Sarcoidosis
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\*\*\*identify condition and what muscle affected? (perimysium or endomysium?) **Skin rash precedes or begins with myositis** * Lilac or heliotrope discoloration of upper eyelids with periorbital edema * Scaling erythematous eruption or dusky red patches over knuckles, elbows, knees (Grotten lesions) **Muscle weakness +/- myalgias** * Slow and symmetrical * Early proximal muscles; late distal muscles * Dysphagia in 1/3 Other: Lung disease, **vasculitis**, myocarditis
Dermatomyositis \*\*Perimysium affected
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**Up to 25% have cancer** •Paraneoplastic syndrome with breast and lung cancer **Juvenile DM: In addition GI involved causing abdominal pain** * GI vasculopathy leads to ulceration, hemorrhage, and perforation * Calcinosis; circumscripta and universalis
Dermatomyosistis **calcinosis circumscripta** localized deposition of calcium in small nodules in subcutaneous tissues or muscle. **calcinosis universalis** widespread deposition of calcium in nodules or plaques in the dermis, panniculus, and muscles.
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Picture - non infectious inflammatory myopathy \*\*Talengentasias of nails \*\*Rash \*\*myalgia
**Dermatomyosistis** (perimysium affected) A, Dermatomyositis. Note the rash affecting the eyelids. B, Dermatomyositis. The histologic appearance of muscle shows perifascicular atrophy of muscle fibers and inflammation. (Courtesy of Dr. Dennis Burns, Department of Pathology, University of Texas Southwestern Medical School, Dallas, TX.) C, Grotten lesions (www.medscape.com)
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* **Systemic inflammatory myopathy; NO rash, endomysium affected** * Muscle weakness +/- myalgias * Early proximal muscles; late distal muscles * Often dysphagia * Other: Lung disease, vasculitis, myocarditis * **Autoantibodies against tRNA synthetases** * +/- ANA positive * **Cytotoxic CD8 +T-cells in endomysium destroy muscle**
Polymyositis; no rash, endmysium
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**\*\*Loose quads** * \> 50 years begins insidiously * Some hereditary * Begins with distal muscles * Begins quadriceps, wrist and finger flexors * May be asymmetric * CD8+ cytotoxic T cells * Intracelluar deposits of **•β-amyloid protien** **•β-pleated sheet fibrils** •Hyperphosphorylated Tau protein
Inclusion Body Myositis
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Differences in inflammatory myopathies 3 types - lymphocytes - respond to immunosuppresant - injury site - begins (proximal or distal) - CK
Picture Diagnosis depends on Clinical symptoms ↑ Creatinine Kinase (CK) EMG: Mixed myopathy and neuropathic findings Biopsy
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Toxic myopathies (3)
* Thyrotoxic * Ethanol * Drug induced
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type of myopathy * Acute or chronic proximal muscle weakness * May precede signs of thyroid dysfunction * Exophthalmic ophthalmoplegia - protrusion of the eyeballs and diplopia due to orbital edema and contracture of the ocular muscles
Thyrotoxic myopathy
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type of myopathy * Cramping/aching muscle; slow movements * Slow reflexes * Proximal weakness eg posterior neck * Elevated CK * Fiber atrophy
Hypothyroidism Myopathy \*\*Head ptosis
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Identify myopathy * Acute rhabdomyolysis after a drinking binge * Painful * Myoglobinuria can lead to renal failure * May be generalized or limited to a group of muscles * May be with alcoholic neuropathy
Ethanol Myopathy
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Durg induced myopathy (3)
**•Steroid myopathy** •Proximal weakness: Atrophy of predominately type 2 fibers **•Chloroquine myopathy** * Proximal weakness * Vacuoles in myocytes **•Statins** •1.5% of users
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* Profound weakness * Associated with corticosteroid therapy * Degraded myosin thick filaments
ICU Myopathy (Myosin deficient myopathy)
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* Neuromuscular Junction Disease: Immune-mediated loss of acetylcholine receptors * Circulating Anti AChR * Decreased AChRs * Thymic hyperplasia: 30% **•Thymoma (an eptihelial neoplasm): 10%**
**Myasthenia Gravis**
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\*\*Loss of Ach receptors. identify condition, treatment and test\*\*\* * Often begins with extraocular muscle weakness * Drooping eyelids * Diplopia * May present with generalized weakness * Weakness variable from minute-minute \*\*Identify pathophys and treatment and test
**Myasthenia Gravis**; **drooping eyelids, diplopia, hard time walking, moment to moment weakness** * _Pathophysiology:_ * Autoantibodies against AChR * Electrophysiology: Decremental decrease in muscle response to repeated stimulus * **Tx**: Thymectomy, anticholinesterase, prednisone, plasmapheresis **Test; Tenselon test - •Short acting anticholenesterase**
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* Neuromuscular junction disorder * Usually paraneoplastic, most commonly from **small cell carcinoma of the lung (almost always a smoker)** * Proximal weakness and autonomic dysfunction * Antibodies inhibit presynaptic calcium channel and **block acetylcholine release (not the receptor compared to myastehernia gravis)** * Enhanced neurotransmission with repetitive stimulation \*\*differentiate from myasternia gravis
**Lambert-Eaton Myasthenic Syndrome** \*\*graph show it gets rapid \*\*myasthernia gravis graph - show decline
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* Name the other structures in the carpal tunnel. * L5 innervates what part of the foot? * Radiculopathy is an upper or lower motor neuron phenomenon?
* Name the other structures in the carpal tunnel. **Flexor digitorium superficialis, flexor digitorum profundus , flexor policis longus, median nerve** * L5 innervates what part of the foot? **Dorsum of foot** * Radiculopathy is an upper or lower motor neuron phenomenon? **lower**
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identify condition •Symptoms –Numbness and tingling to 4th and 5th digits •Exam –Flexion elbow test (positive in 30 seconds), Tinels at elbow •Tests –EMG show reduction of 30% velocity •Treatment (multifold) –Behavior modification (reduce use of armrest), surgical transposition
**Cubital** tunnel sydrome \*\*Compression of ulnar nerve at elbow Ulnar nerve go between the biceps and tricep muscle, behind the medial epicondyle and infornt of the olecranon (elbow). It then dives deep in muscle mass
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•Symptoms –Numbess and tingling to 1-3rd digits, night pain •Exam –Positive phalens, tinels, compression test •Tests –EMG shows 30% velocity decrease •Treatment –Night splints (prevent flexing wrist), steroid injections, carpal tunnel release
Carpal tunnel syndrome \*\*compression of median nerve at the wrist
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what goes through carpal tunnel (4)
Flexor digitorium superficialis Flexor digitorium profundus Flexor policis longus Median nerve
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•Symptoms –Catching of finger when actively flexing finger •Exam –Palpable knot that moves with tendon at distal palm •Tests –None •Treatment –NSAIDS, steroid injections, A1 pulley release
Trigger Finger \*\*•Inflammation of flexor tendon gets it snapping through pulleys in hand.
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identify condition Symptom and exam; inability to straighten finger tip Treatment; Stack splinting \*\*Test and diagnosis
**Mallet finger** ; Laceration of extensor tendon at base of the DP \*\*–**Xray** may show **avulsion fracture at base of DP**
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identify condition - symptoms; pain over radial styloid - treatment; Splint, NSAIDs, steroid injection, release of first dorsal compartment \*\*Diagnosis, condition, exam
**De Quervain Tenosynovitis**; Swelling and inflammation of the tendons that run through the 1st dorsal compartment (APL, EPB). \*\*First dorsal compartment forms one of the borders of the snuff box •Exam –**Finklestein’s test**
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Identify condition * Symptoms –Painless nodules that eventually draw the 4th and 5th digits * Exam –Cords may form, causing flexion of the digits, table top test * Tests –None * Treatment –Splinting, collagenase injections, fasciotomies \*\*what descent of people have this?
**Dupuytren Disease**; Nodular thickening of palmar fascia _(Northern european descent_) \*\*Fold of palmar fascia. Nodules cause digits to flex down
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identify condition of the spine •Tests –No testing for 6 weeks unless atypical pain (night pain, tooth achy pain – indicate neoplasm). Then Xray then MRI. •Treatment –NSAIDs, no bedrest. Then PT
**Low Back Pain** * 80% have no cause * Symptoms –LBP with even a trivial event, radiating to buttocks * Exam –Diffuse LBP to palpation, stiff ROM. Reflexes and neuro exam is Normal\_
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Identify condition of the spine •Symptoms –Usually abrupt, but may be insidious. Unilateral radicular pain, worse with activity •Exam –Straight leg raise, dermatomal weakness and parasthesias \*\*\*\*Diagnosis? Test? treatment
**Herniated Nucleus Pulposis;** Extrusion of center of disc posteriorly, compressing nerve roots. Most common at L4-5 and L5-S1 •**Tests** –Xrays may demonstrate narrowed disk space. MRI is diagnostic **•Treatment** –NSAIDs, rest, then PT, epidural steroid injections, then discectomy
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Describe intervertebral disc structure \*\*what nerve innverates the disc
What’s missing in this pie chart? **Cell!** Also mention that it is largely **avascula**r, receiving nutrients by diffusion from surrounding end-plates; inherently little capacity to heal Not all collagen types are created equal! Type 1 vs Type 2 **Anulus is divided into outer and inner layers** with outer layer having highest tensile load to prevent bulging. **Sinuvertebral nerve innervates disc**
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identify lumbosacral dermatones - what innervates; umbilicus? patella reflex? dorsum of foot? back of foot?
T10 – umbilicus L4- patella reflex L5 – dorsum of foot S1,S2; back of foot (achilles heel)
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identify condition of the spine •Symptoms –Back pain with bending. May cause claudication •Exam –Dermatomal weakness, may feel spinous process stepoffs. \*\*identify condition, tests, treatmnet
**Spondylolisthesis**; Forward slippage of lumbar vertebral body. * Tests –Flexion / extension **Xrays** of spine show **slippage** * Treatment –NSAIDs, surgical fusion
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Identify condition
**Spondylolisthesis** (forward slippage of lumbar vertebral body) - L4 slipped forward compared to L5 - Kink cause nerve root compression - Can also have pars defect (slippage more liekly to occur – stress fractures or congenital)
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Describe Lumbar spine anatomy - what is axial load distribution during weight bearing - in anterior vs posterior, which has less mobility and greater stiffness ? which allow for mobility? - function of posterior spine
Review anatomy again, point out axial load distribution **(80/20)** during weight bearing. **Anterior spine** has **_less mobility and greater stiffness_** than posterior elements and mainly function to bear load. **Posterior spine** functions to p**_rotect the neural elements and allow for mobility._**
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identify condition •Symptoms –Achy pain in spine, worse with ROM •Exam –Tender to palpation, stiffness, radicular or myelopathy may be present •Tests –Xrays show osteophytes and sclerosis. MRI can show pinched nerves •Treatment –NSAIDs, Steroids (foramenal injection), Traction, surgical decompression and fusion
**Spondylosis**; Degenerative changes in the facets or discs leading to osteophytes and possible nerve compression \*\*\*Osteophytes cause foramenal stenosis from facet arthritis
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identify condition of the spine
**Spondylosis** •Degenerative changes in the facets or discs leading to **osteophytes and possible nerve compression**
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identify the cervical dermatomes - ear - front part of arm - thumb - first 2 digits - last 2 digits
**Cervical dermatomes** C2 – ear C5 – front part of arm C6 – thumb C7 – first 2 digits C8 – last 2 digits
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Cervical myotomes from C5 to T1 (identify)
* C5 – Deltoid * C6 – Biceps, wrist extensors * C7 – Triceps, wrist flexors * C8 – Finger flexors * T1 – Interossei
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Identify condition •Symptoms –Stiff spine, pain •Exam –**Stiff spine** •Tests –Xrays show bridging osteophytes over 4 vertebra, no HLA association •Treatment –NSAIDs
**DISH** - Idiopathic disease characterized by **osteophyte formation spanning several vertebra**
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Identify condition and treatment •Symptoms –Unilateral radiating dermatomal pain •Exam –ROM causes radiating pain, dermatomal weakness and parasthesias. **No upper motor neuron signs** •Tests –MRI shows **Nerve root Compression**
**Radiculopathy** ; compression of nerve root •Treatment –NSAIDs, steroid injections, PT traction. Surgical decompression \*\*Lumbar radiculopathy is a symptom not a cause. It can be caused by HNP, spondylothesis, spondylosis.
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Identify condition and treatment •Symptoms –Bilateral weakness, difficulty with fine motor tasks, wide based gait •Exam –Bowel or bladder dysfunction, **upper motor neuron signs** •Tests –MRI shows **cord compression**
Myelopathy; compression of the spinal cord •Treatment –Epidural injections may help, but surgical decompression is recommended due to risk of permanent deficits
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1. Ulnar nerve innevates what parts of the hand? 2. which cervical nerve root innervates the deltoid? 3. what are the structures in the first dorsal compartment
1. **Ulnar nerve** **- Hypothenar muscles** (a group of muscles associated with the **little finger**) - Medial two lumbricals. - Adductor pollicis. - Palmar and dorsal interossei of the hand. - Palmaris brevis. 2. Which cervical nerve root innervates the deltoid? **C5** 3. What are the structures in the first dorsal compartment of the hand? **abductor pollicis longus (APL) and the extensor pollicis brevis (EPB)**
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In mid-july, 72 y.o man with PMH of HTN, CAD and CHF presents to hospital with 3 days of **fever, chills, body aches**. Temp 100.8. Took some ibuprofen but no relief. Meds – losartasn, Lasix, carvedilol and atorvastatin. **Lives in WV** Labs; CBC (low platelets (90x109) – thrombocytopenia, low hgb (9.4) – anemia, WBC – 6 x 109) , blood culture CHEM Test (electrolytes). ASL/ALT levels elevated **Peripheral smear; hemolytic anemia – MALTESE CROSS** **\*\***Identify - diagnosis, vector, form of disease? (mild or sever), treatment?
**Babesiosis (not travelled outside US)** Treatment; **Mild disease: Atovaquone PLUS azithromycin** Vector – Blacklegged **tick (Ixodes** scapularis) in eastern US.
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**19 y.o male**. Presumed **pneumonia and thrush** (white exudates on tongue). NEW rash. Vitals; T 104, Pulse 120, BP 108/68. R 22; tachycardia, acute distress, diaphoretic Tests; Sputum culture, CXR (possible right lower lobe infiltrate) – repeaded again and shown bilateral fluffy/**patchy infiltrates – suggest ARDS (acute respiratory distress syndrome)** **Sepsis – hypotension, tachycardia, fever or no fever, tachypnea** Social history; goes out fishing and hunting and shoots squirrels in Kentucky. Lives in dorm with 3 other students. \*\*\*Identify diagnosis and treatment, vector
**RMSF (Rocky mountain Spotted Fever) -** Rickettsia rickettsii **treat with DOXYCYCLINE**. RMSF; caused by rocky mountain wood tick (dermacentor andersoni), Colorado tick fever and tularemia.
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Identify * Weakly gram-negative bacilli * Cell was structure like Gram-neg rods, but… –Peptidoglycan layer is minimal –LPS has weak endotoxin activity –So, no beta-lactams for treatment here * Obligate intracellular * Replicate in cytoplasm of cells * Difficult to see in tissues→ special stains needed (Giemsa, Gimenez) \*\*Identify 4 species
**Rickettsia** •4 species that are important human pathogens: –**R. rickettsii;** RMSF - **R.akari;** rickettsialpox (infected mites) - **R prowazekii;** louse borne typhus and flying squirrels (vasculitiss) - **R typhi;** endemic (murine) typhus - rodents
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5 DON'Ts of rickettsial disease
* DON’T wait for a petechial rash to develop to suspect the diagnosis * DON’T exclude the diagnosis because there is no history of tick bite * DON’T exclude the diagnosis solely for geographic or seasonal reasons * DON’T withhold therapy if you are clinically suspicious * DON’T be afraid to use doxycycline at any age
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Identify rickettsia type * Outer membrane protein A **(Omp A)** is a pathogenic factor→ adherence to endothelial cells * Replication in cytoplasm and nucleus results in **vasculitis** * Intracellular growth protects the bacteria from immune clearance \*\*\***Most common rickettsia** \*\* Identify vectors
**Rickettsia rickettsii** * _Seasonal_: 90% of infections occur from April-September (greatest tick activity) * Vectors: Ticks (Ixodeae family) –Dermacentor andersoni: **wood tick** (Rocky mountain states) - Dermacentor variabilis: **dog tick** (SE US) \*\*The highest incidence rates, ranging from 19 to 63 cases per million persons were found in **Arkansas, Delaware, Missouri, North Carolina, Oklahoma, and Tennessee.**
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Identify condition based on clinical manifestation (labs) * Incubation: 2-14 days * Fever, chills, headaches, myalgias * Pathognomonic rash appears late: after 3-5 days –**Centripetal, palms and soles** –But not on all patients * Abdominal pain, vomiting, hepatitis * Respiratory failure, encephalitis, renal failure, hypotension, myocarditis * **Fatal in 20% of untreated cases**→ clinical suspicion is key!
RMSF clinical manifesttaion s \*\*Fever, chiils, headach, myalgias, **centripetal RASH (appears late - from periphery to center)**, respiratory failure, hypotension, myocarditis, encephalitis, renal failure, hepatitis * Thrombocytopenia, coagulopathy * Anemia * Normal WBC count * Hyponatremia * Transaminitis * **Remember! Diagnosis before the onset of the rash is clinical AND epidemiologic**
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How to detect RMSF labwise 1. acute phase RMSF (2) 2. what can also be employed for detection, however an antibody response may not be detectable in initial samples, and paired acute and convalescent samples are essential for confirmation 3. Laboratory confirmation \*\*what test lack specificty
1. Acute phase - PCR and imunohistochemical methods in skin biopsy specimens 2. serology 3. lab confomation of RMSF * Fourfold change in IgG\* specific titer reactive with R.rickettsii by indirect immunofluorescence assay (IFA) between paired serum specimens (one taken in the 1st week of illness and a second 2-4 weeks later), or * Detection of R. rickettsii DNA in a clinical specimen via amplification of a specific target by PCR assay, or * Demonstration of rickettsial antigen in a biopsy or autopsy specimen by IHC, or * Isolation of R. rickettsii from a clinical specimen in cell culture \*\*\*\***IgM tests lack specificity and are usually false +**
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identfiy ricketssia type (describe 2 phases) * Rickettsialpox * Cosmopolitan * Transmitted by infected mites * Reservoir: rodents (common house mouse) * Humans are accidental hosts when bitten by infected mites
**R.Akari; ricketssialpox** •_Biphasic presentation_ **•First phase** –1 week after bite: **papule to ulcer to eschar** at the site of the bite * Incubation for 7-24 days, systemic spread * **Then, 2nd phase** –**High fever, severe headache, photophobia, papulo-vesicular rash, with pox-like progression** (vesicles that then crust over) –Milder course than RMSF –Complete healing within 2-3 weeks
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identify type of ricketssia based on transmission * During a blood meal, the louse defecates highly infective feces at the site of its feeding * Rickettsiae present in louse feces may then be introduced into abraded or injured skin or mucous membranes by either scratching or hand contamination * Lice feces may remain infectious for as long as 100 days→ human to human transmission can occur from sharing clothes
Rickettsia prowazekii •Epidemic (louse-borne) typhus –Humans are the principal reservoir –Pediculus humanus (body louse) –disasters, war, famine –Rare in USA •In USA sporadic disease→ “flying squirrels” –squirrels have fleas –fleas bite humans
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•2 syndromes –Acute, potentially severe vasculitis (7-14 days after contact with infected lice) •Fever, centrifugal maculopapular rash, CNS symptoms –Recrudescent form (Brill-Zinsser disease) 10-50 years after primary infection •Milder form, rash, flu-like symptoms, seen in elderly patients (WWII refugees) §Diagnosis: serology (MIF test)
Rickettsia prowazekii
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* American Boutonneuse fever/ Tidewater spotted fever * Recently described (index case in 2002) * Geo: mainly southern United States (VA) * Vector: Amblyomma maculatum (Gulf coast tick) * Fever, headache, myalgias **•Typically several eschars and rash on PE** * Mortality is low * Dx: serology, PCR, culture from skin biopsy **•Rx: doxycycline**
Rickettsia parkeri
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* Generally mild * Non-specific symptoms –Fever, headache, chills, myalgias –Rash (variable presentation) §Dx: serology by IFA §As with other rickettsial diseases, early reliable diagnosis is not possible→ clinical presentation + epidemiologic setting are key!
Rickettsia typhi * Endemic (murine) typhus * Worldwide, more in warm, humid areas * Reservoir: rodents * Main vector: Xenopsylla cheopis (rat flea) –Also cat flea, esp in USA •Humans are infected by inoculation of infective flea feces in bite wounds
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identify treatment of ricketssia and oriental infections
**•Doxycycline is the drug of choice** * Chloramphenicol or a fluoroquinolone are alternative drugs * Prompt diagnosis is key! * **Empiric treatment with doxycycline should be started as soon as it is suspected…do NOT wait for confirmatory serology**
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Treatment of pediatirc RMSF?
•Doxycycline usually recommended only for treating children \>8 years –Dental staining/enamel hypoplasia **•For RMSF, doxycycline is the drug of choice, regardless of the age of the patient!** –Not much clinical data on use of other drugs –Case fatality of 30% if untreated
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identify (2) * Obligate intracellular bacteria * No peptidoglycan or LPS –Beta-lactams do not work for treatment! * Grow on hematopoietic cells * Replicate in phagosomes of host cells
**Ehrlichia and Anaplasma** * Morula: microcolony of Ehrlichiae within a vacuole * Ehrlichia chaffeensis→ human monocytic ehrlichiosis (HME) * Anaplasma phagocytophilum →human granulocytic anaplasmosis (HGA)
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identify * Reservoir: deer, dogs * Vector: ticks (Amblyomma americanum ) * Predominantly Southeast, South central and Midwest states * 1-3 weeks after tick bite→ flu-like illness * Late-onset (1 week after) rash (spares hands and feet) * Mortality 3% * Dx –serology by IFA (paired specimens to see ↑ in IgG) –PCR in blood –Peripheral blood (Giemsa) to see morulae in monocytes is insensitive
**Ehrlichia chaffeensis** The areas from which cases are reported correspond with the known geographic distribution of the lonestar tick (Amblyomma americanum), **3 states (Oklahoma, Missouri, Arkansas) account for 30% of all reported E. chaffeensis infections**
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Identify * Reservoir: deer, sheep, rodents * Vector: hard-shelled ticks ( Ixodes scapularis and pacificus) * Predominantly Northeast/north-central states and Northern California * 1-3 weeks after tick bite→ flu-like illness * Late-onset (1 week after) rash (spares hands and feet) * Mortality 1% * Dx –serology by IFA (paired specimens to see ↑ in IgG) –Blood PCR –Peripheral blood (Giemsa) to see morulae in granulocytes is insensitive
**Anaplasma phagocyphilum** The highest incidence rates, ranging from 3.1 to 136 cases per million persons were found in Delaware, Maine, Minnesota, New Hampshire, New Jersey, New York, Rhode Island, Vermont and Wisconsin
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identify lab finding in anaplasma and ehrlichia - WBC count - lymphocytes - plateles - liver \*\*treatment and prevention
* Leukopenia * Lymphopenia * Thrombocytopenia * Elevated liver enzymes **•Doxycycline is drug of choice, regardless of patient’s age** * Failure to respond to doxycycline within 3 days suggest infection with other organisms! * Prevention and Control –clothing –insect repellants –inspection and prompt removal of ticks
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identify 3 types and what they cause * Weakly staining, gram Neg spirochetes * Motile (flagella) * Very difficult to cultivate
**Borrelia** * B. recurrentis→ Epidemic relapsing fever * Borrelia spp→ Endemic relapsing fever **•B. burgdorferi→ Lyme disease**
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identify * 3 principal foci: Northeast, Minnesotta and Wisconsin * Vector: Ixodes scapularis and pacificus * Reservoir: white-footed mouse and white-tailed deer. transmitted in tick's saliva * Incubation period up to 1 month from tick bite \*\*Identify 3 stages of disease manifestation
**Borrelia burgdorferi=Lyme disease** •3 stages –Early **localized**→ distinctive **rash**: erythema migrans (**bull’s eye**) –Early **disseminated**→ multiple **EM, meningitis**, cranial nerve abnormalities such as **Bells palsy and carditis** –**Late** disease→ **encephalitis and arthritis** (esp knees) \*\*Chronic lyme disease; fatigue, joint pains and cognitice problems. \*\*\*No clinical or biological definition so not a recgnized disease
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How do you diagnose lyme disease (borrelial burgdorferi) \*\*2 steps (specific vs not very specific) - best way to diagnose?
* For early stage, **Dx is best made clinically** since Ig are not detectable within the 1st 4 weeks of infection * 2-step approach * EIA or IFA (highly sensitive, not very specific) **•Confirmatory Western Blot (very specific)** •Always remember: clinical picture and epidemiology –→ Do not send serologic tests in patients with unspecific symptoms!
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Treatmenet of lyme disease \*\*Based on? - associated conditions tp treat (CNS, carditis, recurrent arthritis)
Treatment of Lyme disease is based on age * Amoxicillin or cefuroxime for **children \<8 y** * Doxycycline for **≥ 8 years** * Ceftriaxone for CNS, carditis or recurrent arthritis
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Identify (condition, area, treatment) * Rash typical of erythema migrans and mild flu-like symptoms in non-Lyme endemic areas * Associated with a bite by the Lone Star tick (A. americanum) * Preliminary studies show the cause is postulated to be a spirochete: B. lonestari – PCR on ticks, but has not been fully confirmed
**STARI - Southern Tick-associated Rash Illness** * STARI have been described in patients from Missouri, Maryland, Georgia, South Carolina, and North Carolina (**Non - lyme endemic areas)** * All three stages of the A. americanum tick feed on **white-tailed deer,** which may serve as the **reservoir** for this infection \*\*Treatment same as Lyme disease - Doxycyclie and amoxicillin
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identify cndition (epidemic vs endemic) •Incubation of **1 week** **•Biphasic** –1) Fever, chills, headaches, hepatosplenomegaly * Afebrile period of 1 week * **Return of symptoms** * Relapses * Mortality as high as 40% * Dx: –**Giemsa** on peripheral blood during febrile episode –Serology NOT useful because Borrelia undergo antigenic phase variation, also cross-reaction with other spirochetes §Treatment §Doxycycline §Penicillin and erythromycin for pregnant and children under 8 y
**Borrelia - Relapsing fever** **•Epidemic (louse borne)** –B. recurrentis –Natural disasters, unsanitary conditions **•Endemic tick borne (soft-shelled)** –Borrelia spp. –Reservoir: rodents, small mammals –Ticks feed nocturnally and contaminate the wound with saliva and feces that are infectious –Bite is painless: goes unnoticed
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Identify condition Not a bacteria but protoza •Forms: –Sporozoite (ticks), trophozoite→merozoite→gamete **•Intra-erythrocytic parasite** **–Yes, like malaria!**
Babesia - patients can have co-infections of lyme and babesia •But both Babesia and B. burgdorferi share the same vector (Ixodes tick) and reservoir (white footed mouse) - Babesia microti is the most common species
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Identify condition based on manifestation - range from subclinical to life threatening **•Hemolytic anemia** * **Influenza-like symptoms (e.g. , fever, chills, body aches, weakness, fatigue)** * Splenomegaly, hepatomegaly, or jaundice * More **severe in immunocompromised states**
**Babesia** •**Risk factors for severe babesiosis include:** asplenia, advanced age, and other causes of **impaired immune function** (e.g. , HIV, malignancy, corticosteroid therapy)
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identify cndition based on lab finding (patient has **hemolytic anemia, fever, chills, myalgia**) * Parasites can be detected by microscopic examination of blood smears –**Maltese cross** * PCR can be used to detect low levels of parasites * Serology not helpful (cannot distinguish between acute versus old infection) \*\*Identify treatment in mild vs severe form
**Babesiosis** •Examination by a reference laboratory should be considered for confirmation of the diagnosis, in part because it can be difficult to **distinguish between Babesia and Plasmodium** Treatment - COMBINATION THERAPY * Mild disease: Atovaquone PLUS azithromycin * Severe disease: Clindamycin PLUS quinine
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1. identify 2 urgent meidal managemnts of open fractures 2. What imaging is most sensitive to fracture 3. what bone graft is osteogenic, osteroinducive and osteoconductive
* 1. For _open fractures_, name two urgent medical managements. **Tetanus and Abx.** Semi- urgent treatment is surgical debridement * 2. What imagine modality is _most sensitive for fractures_? **MRI** **3. AUTOGRAPT** is all 3 - osteogenic (contain viable osteoblast), osteoinductive (stimulation) and osteoconductive (bone scaffold) \*\***Osteogenic (autologous graft** – contain viable osteoblasts), **osteoinductive (BMP 2 and BMP 7** – bone morphogenic protein - stimulation), and **osteoconductive? (cancellous allograft**- bone scaffold)
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Fracture Principles History; acute vs stress fracture PE; presentation? check skin for? if high energy - evaluate for?
**•History** –**Acute fractures** are associated with **trauma, sometimes high energy** –**Stress fractures** have **insidious onset of pain,** particularly with weight bearing/activity **•Physical Exam** –Tenderness, swelling, deformity, crepitation, and abnormal movement –Must **examine skin for ANY breaks**, regional joint stability, and nerve and vessels for injury. **–If high energy**, must evaluate other limbs and spine for **occult injury**
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Fracture workup 1. best imaging to order 2. what is used for difficult 3-D fractures 3. which is most sensitive
**–X-rays are the best test to order** •Stress fractures may take 1-4 weeks to show up on X-ray **–CT Scans** indicated for **difficult 3-D fractures** (elbow, tibia plateau fx) –**MRI most sensitive** for fractures (nondisplaced femoral neck); we don’t do this immediately because it is expensive – do xray first.
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Identify 4 R's in the treatment of fractures
**–Recognition** •When in doubt, get an X-ray **–Reduce** •“Set” the bone straight, either with manipulation or surgery **–Retain** •Keep the reduction either with a cast or surgery (implants) **–Rehab** (during and after healing process) •Balance between stability and stiffness
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complications of fracture 1. term for bone that don't heal 2. bone heals in wrong alignment 3. enlarge muscle compress vasculature 4. emergency condition that must be repaired or bypassed
**–Nonunion** •Bone _does not heal_ **–Malunion** •Bone _heals in unacceptable alignment_ (need to do intentional fracture and re-reduce it) **–Compartment Syndrome** (treat with _immediate fasciotomy_) •**Swelling from soft tissue damage compresses nerves and vessels, causing permanent damage.** Must loosen clothing / wraps / etc to make sure that is not the cause of constriction. **EMERGENCY!** **–Nerve and Vessel damage** •Must be repaired or bypassed. **EMERGENCY!**
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identify 2 forms of fracture healing (type of ossification) 1. Rigid fixation from plates. Direct healing - no callous. 2. Indirect formation of bone from uncommited mesenchymal cells. osteoblasts form new osteoid. \*\*\*3 stages timeline for inflamation? repair? remodel?
**•Primary _(Intramembranous)_** –Rigid Fixation from Plates –Direct healing with no callous **•Secondary _(Enchondral)_** –Controlled motion (**Rods, Casts**) –Indirect formation of bone from uncommitted mesenchymal cells (form ossified callous) **–Three stages** * Inflammatory for 48 hours * **Reparative** for 8 weeks (this is how kids grow through growth plates) * Remodeling for 1 year
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Identify fracture healing –Lack of radiographic evidence of progression of callus formation over a 3-5 month period –Risk factors * Smoking * Infection (occult infection) * Poor immobilization * Malnutrition (low vitamin D levels, low calcium) * NSAID * Poor blood supply (fracture close to blood suppy) * High energy trauma (high energy open femur fracture)
**Nonunion**
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3 types of bone grapft
**–Osteogenic** * Bone forming * Only autologous bone graft contains viable osteoblasts. **–Osteoinductive** * Bone stimulation * Encourages differentiation of mesenchymal cells into osteoblasts * BMP-2 and BMP-7 (bone morphogenic protein) **–Osteoconductive** * Bone scaffold * Cancellous allograft
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Bone graft - which is osteogenic, conductive and inductive - which is conductive only - which is inductive, expensive and not conductive - whcih is inductive and conductive but expensive - which is inductive but very expensive
–**Autografts** from cancellous pelvis is genic, inductive and conductive, but painful –**Allografts** are conductive only, and carry infection risk. –**Demineralized bone matrix** are inductive, but expensive and not conductive –**Synthetic substitutes** are inductive and conductive, good compressive strength, but very expensive –**BMPs** are inductive but very expensive.
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2 groups of Treatment option of fracture type 1. involves joint surface 2. Does not involve joint surface
**1. Intra-articular** –Involves joint surface –Needs perfect reduction –Early motion key **2. Extra-articular** –Does not involve the joint surface –Needs good overall alignment
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Identify 6 treatment options of fracture 1. **undisturbed** fracture milleu, _no reduction_, **stiffness** 2. **Undistubed**, **_poor reduction,_** fracture disease, pin site problems 3. reduction, _stripping_ (increase nonunion), **load sharing. _bigger wounds_** 4. No reduction (less stripping), fracture disease (less stripping), **load bearing. smaller wounds** 5. not anatomic, less stripping (too many screws lead to less healing), **load bearing. small wound** 6. fracture milleu is OK, no stiffness due to early mobility, pin site issue and it is a pain in ass, **load bearing. small incision**
1. **Cast;** undisturbed fracture milleu, no reduction, stiffness 2. **Traction;** Undistubed, poor reduction, fracture disease, pin site problems 3. **ORIF**; reduction, stripping (increase nonunion), **load sharing. bigger wounds** 4. **ORIF locking** (like an internal Ex Fix); No reduction (less stripping), fracture disease (less stripping), **load bearing**. small wound 5. **Intramedullary Nail (IM nailing)**; not anatomic, less stripping (too many screws lead to less healing), **load bearing. small wound** 6. **Ex. Fix;** fracture milleu is OK, no stiffness due to early mobility, pin site issue and it is a pain in ass, **load bearing. small incision**
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identify pro (4) and con (2) of **casting** ## Footnote **\*\*what type of bon ehealing occurs?**
**CASTING** •Pro –Undisturbed fracture milleu –No incisions –We are gardeners, not carpenters –Heals by **endochondral ossification (secondary healing)** **•Cells differentiate into chondrocytes and lay down cartilage which calcifies. Osteoclasts absorb this cartilage and osteoblasts lay down new osteoid** •Con –No anatomic reduction –Stiffness
291
Identify pro (2) and con (3) of traction
**Traction** Pro Doesn’t disturb fracture milleu No risk of surgery Con Poor reduction Pin site problems Fracture Disease
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Pro (4) and con (3) of IM (intramedullary nailing)
IM Nailing •Pro –Load bearing –Small incisions **–Periosteal blood supply ok** **–Stimulates endosteal blood supply** •Con –Not anatomic –**Callus formation** –Too much movement?
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Identify pro(4) and con (2) of ORIF
ORIF - open reduction internal fixation •Pro –Anatomic reduction –Load sharing –Early motion –Heals with intramembranous ossification •Undifferentiated cells become osteoclasts and lay down new osteoid. – •Con –Stripping increases nonunion –Bigger wounds
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identify •Pro –Load Bearing –Internal ExFix –Early Motion –Less Stripping –Smaller wounds –Good for poor bone quality •Con –Decreased healing due to lack of micromotion –Cost –Not anatomic reduction
ORIF Locked
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Pro (2) vs con (1) of **weight bearing status - less movement** (race against fatigue failure)
•Pro –Quicker return to function –Stimulates bone growth •Con –May be more weight than fixation can handle
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297
Pro (4) vs con (2) of movement (after fracture treatment)
•Pro –Faster return to function –Decrease stiffness –Faster healing –Helps reduction of fractures •Con –Wound problems –May overwhelm fixation or repair
298
1. describe compartment syndrome 2. define non-union 3. are IM nails load sharing
* 1. Describe compartment syndrome. Swelling from soft tissue damage compresses nerves and vessels, causing permanent damage. Must loosen clothing / wraps / etc to make sure that is not the cause of constriction. EMERGENCY! * 2. Define Non-union; lack of healing. Lack of radiographic evidence of progression of callus formation over a 3-5 month period * 3. Are IM Nails load sharing? No – load bearing
299
1. where does majority of growth come from in lower extremity 2. risk factors of non-accidental trauma 3. 2 tests to evaluate hip dysplasia
* Where does the majority of growth come from in the lower extremities? **Knee** * What are the risk factors for non-accidental trauma? Child abuse - **Low income, first born, premature, stepchildren, handicapped, single parent, drug use, unemployed parents, abused parents**. * Name two tests for evaluating hip dysplasia? **Barlow (adduct) and Ortolani (abduct) exam**
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Identify condition and treatment —Symptoms; **Girls 7 times more likely to progress** **¡No pain. Ill fitting clothes** —Exam **¡Forward bend test** —Tests ¡Full length Xrays **measure vertebral angle**
**Scoliosis**; _**Lateral curvature** greater than 10deg_, often associated with rotational deformity. M:F = 1:1 of curves less than 20, but girls are 7 times more likely to progress —Treatment **Brace** if angle \>30. **Surgery** if \>40-50
301
Identify condition and treatment —characterized by **plantar flexion of ankle (varus type); adduction of the heel; high arch; adduction of the forefoot** —Symptoms ¡None —Exam ¡Rule out neurological problems, **foot** looks like as described above. **Rigid** —Tests ¡None
**Club Foot** (Varus type) —Treatment (goal of treatment is to **provide rigid free foot**) ¡**Manipulation** and **casting** _immediately_. **Surgery if still rigid at 3 years.**
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Identify condition and treatment —**Overuse injury causing apophyseal injury at tibial tubercle.** —Symptoms **¡Pain over tibial tubercle** —Exam ¡Pain over tibial tubercle —Tests ¡Xrays show **fragmentation of tubercle**
**Osgood Schlatter** —Treatment **¡NSAIDs, rest, PT**
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Identify condition and treatment **—associated with ligamentous laxity, left hip, female gender, breech presentation** —Symptoms **¡Limp?** —Exam **¡Barlow and Ortolani exam** * Barlow test – adduct let inward (dislocate hip) * Ortolani – abduct the hip (relocate hip) —Tests **¡Ultrasound can help with difficult cases**
**_Hip dysplasia_**; **—Malformed hip socket and femoral head, associated with ligamentous laxity, left hip, female gender, breech presentation** **\*\***Hip socket don’t form fully so you have shallow acetabulum with damaged cartilage – osteoarthritis —Treatment **¡Pavlik Harness** to _force relocation_ of hip. **Casting and surgery in older kids**
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identify condition and treatment —Symptoms **¡Limp and stiffness** —Exam **¡Decreased internal rotation and abduction** —Tests **¡Xrays** show **sclerosis, coxa magna**. MRI can help with diagnosis
**Perthes Disease** —**Idiopathic osteonecrosis of femoral head, between 4-8 yo**. —Treatment ¡**ROM and bracing**. No good treatment.
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Identify condition and treatment —, associated with **obesity, males, sports, endocrine disorders** —Symptoms ¡**Pain with activity** —Exam ¡**Loss of internal rotation with hip flexed** —Tests ¡AP and Lateral **Xrays show slip**. Workup for **endocrine abnormality** if bilateral
**SCFE** (_Slipped capital femoral Epiphysis)_; —**Displacement of the femoral head through the physis ususally during growth spurt**, associated with obesity, males, sports, endocrine disorders —Treatment ¡**Surgical fixation in situ**
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Identify condition —Symptoms ¡**Worried parents** —Exam ¡**Measure knee angle** —Tests ¡Weight bearing Xrays if outside normal —Treatment ¡**Observation, bracing, occasional epiphyseal stapling, osteotomy**
Genu Varum / Valgum; Normally, the knee starts at birth in varum 10-15deg, and by 18 months straightens out to 0. Maximum valgum of 15 deg at age 4, then 5-10 deg in adolescence. **Valgus** – **knocked knee** (Gus has knocked knee) **Varus** – **bow leg** (Riri has a bow leg)
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Identify condition and treatment —Symptoms ¡**Pain, limp, frequent ankle sprains** —Exam ¡**Restricted hindfoot movement** —Tests ¡**Xrays will show navicular coalition**. _CT scan_ can confirm
**Tarsal Coalition**; Abnormal connection between tarsal bones
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Identify condition —Symptoms ¡Limp, refuses to walk, groin pain. History of viral infection elsewhere —Exam ¡Limp, stiffness. afebrile —Tests ¡Xrays show effusion. CBC, ESR, CRP are not elevated. Joint aspirate \< 50000 WBC. Gets better with NSAIDs —Treatment
Transient synovitis of the hip; sterile effusion of hip causing pain \*\*Treatmnet - supportive care \*\*rule out septic arthritis
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Identify condition and treatment —**Affects 2-12 yo, most common elbow fracture** —Symptoms ¡**Fall of trampoline, elbow deformity, pain** —Exam ¡Neurovascular exam important. —Tests Xrays , **positive posterior sail sign**
**Supracondylar Humerus Fracture** —Treatment ¡Casting vs surgical reduction
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Identify condition and treatment —Symptoms **¡Pain in legs** —Exam ¡**Bowed legs (genu varum)** —X-rays ¡Looser lines (osteoid seam) ¡Widened growth plates —Labs **¡Low normal serum Ca, Phos low**
**Rickets**; —Error in Vit D metabolism causes failure of mineralization (cause by 3 things - **hypocalcemia or hypophosphatemia or vit D deficiency**) —Treatment ¡Nutritional supplementation, treat underlying cause (meds, —BS **¡Hypertrophic zone is large\_** ¡Vit D Pathway; **– if you eat vit D you get D2 and D3 – then broken down to 25-hydroxy vit D (lungs) and 2 kidney forms.**
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what part of UE and LE gets most of the growth
**LE;** most growth in the **knee** 70% of femur growth in distal 55% tibia is proximal **UE**; most growth in the **shoulder/wrist (proximal)** not elbow 80% humerus proximal 75% radius distal
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identify condition (incidence and treatment) —Risk factors: ¡Low income, first born, premature, stepchildren, handicapped, single parent, drug use, unemployed parents, abused parents. —Fractures in non ambulatory children —Pay attention to the pattern of injury: ¡Posterior rib fractures (shaky baby) ¡Spiral fractures (low energy mechanism) ¡Metaphyseal corner fractures ( pathopneumonic for non-accidental trauma)
**Non accidental trauma** **—Incidence:** ¡42/1000 children were victims of abuse or neglect ¡15-20% present with fractures ¡**Humerus is the most common bone, then femur** **—Treatment** ¡Contact CPS ¡Rule out other causes (OI, hemophilia, Caffey’s disease, leukemia, accidental trauma) ¡Treat fracture
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Identify classification of growth plate injuries (type I to IV)
Salter Harris Classification Type I – fracture through the growth plate TYpe II – growth plate + metaphysis Type III – growth plate and epiphyseal Type IV – both Type V – Crush injury
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Identify condition * Mono articular * Oligoarticular * Systemic symptoms * JIA (painless single joint), Lyme, Septic * Ophthalmology consult? * Sometimes painless
Acute joint effusion (knocked knee)
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Identify condition —**Permanent, non-progressive brain injury in the peripartum period.** —Upper motor neurons affected, with spasticity —Hemiplegia; Diplegia —Keeping mobile is key – for as long as possible —Be suspicious for cerebral palsy in a patient with delayed motor development, history of prematurity, prolonged NICU stay, Toe walking.
Cerebral Palsy
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Identify condition and **mutation** \*\*\* * Disproportionate short stature (**most common cause of dwarfism)** * **Autosomal Dominant** * **Hypertrophic zone in growth plate is _narrow_** * Problems involve the spine
Achondroplasia **_•FGFR-3 Mutation_**
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Identify condition **- fibrillin mutation\*\*\*\*** \*\***Long fingers and narrow bones**
**Marfan's Syndrome**
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identfiy condition and treatment * **Defect in collagen I from osteoblasts** * Sx **•Blue sclerae,** macrocephaly, **hearing loss**, **poor dentition**, kyphoscoliosis, fracture, **growth retardation**
**Osteogenesis Imperfecta** Treatment; •**Bisphosphonates, surgery**
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1. genetic mutation of achondroplasiia 2. vitamin deficiency of rickets 3. risk factors of SCFE (slippec carpital femoral epiphysis)
* What is the genetic mutation for **achondroplasia? FGFR-3 mutation** * What Vitamin is deficient in **Rickets? Vitamin D** * What are the risk factors for **SCFE** (slipped carpital femoral epiphysis)? associated with **obesity, males, sports, endocrine disorders**
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CASE 1 (identify condition, workup, enzyme at play, treatment) **Left Knee pain.** 25 y.o with **sickle cell anemia** with severe left knee pain for **12 hours**. Happened once before where he got medications that made him feel better PMH; sickle cell anemia SH; EtoH, tobacco, **sex “when he can get it”** **Xray;** left knee of skeletally mature individual. **Normal** Tests; **Fever of 100**
SEPTIC ARTHRITIS PATIENT RESULTS; labs; **ESR 50 (high)**, CRP (20). WBC = 20,000. **Knee Aspirate = 100,000** WBCs/mm3. All confirm **SEPTIC ARTHRITIS. \*\*Joint aspirat \>5,000** Treatment; Emergent washout, Culture grew **gonorrhea,** started on abx. In SEPTIC ARTHRITIS; **METALLOPROTEASES** cause permanent destruction in about 8-12 hours which can lead to **loss of articular cartilage.**
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Case 2 CC**; Bilateral hip pain 3 years** HPI; 50 y.o hx of **groin pain in both hips.** Hurts all day and stiff on movement. **Feels better after 1 hour.** Swelling in both wrists and knees but no pain knee. High pain tolerance. Tired of pain PMH; HTN, Obesity, high cholesterol in blood, DM II SH; None FH; **joint pain runs in family.** Physical exam; Pleasantly plump. Painful groin pain to full ROM. No ulnar deviation to fingers. **Slight limp. Some effusion in knees and wrists but they are pain free.** No nodules on fingers. MCP are boggy.
**RHEUMATOID ARTHRITIS** - refer to rheumatology – started **Embel (etanercept)** RA (NSAIDS, DMARDS, Steroid).
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Case 3 CC; **right knee pain of 3 months.** HPI; **19 y,o** right knee pain since a fight 3 months ago. Thought it was bruise but pain got progressively worse. **Toothachy night time pain**. No longer relieved by NSAIDS. No pain radiation Physical exam; **swelling in distal femur.** ROM knee 15-90. **No McMurray’s sign (test for meniscal tear)**. NVI distally (neurovascular intact)
**Osteosarcoma – Neoadjuvant chemo (doxorubicin, cisplatin, MTX),** wide resection, reconstruction and chemo.
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Case 2.1 CC; **42 y.o female Leg pain for 3 days**. Sudden onset severe sharp, stabbing, burning pain in **posterolateral leg extending into lateral fot,** imporved by leaning to opposite side. Patient was **lifting a box when it happened**. Pt has numbness and tingling. No constitutional symptoms (fever, sweats, chills, unexplained weight loss). PMH/PSH; HTN. Tubal ligation SH; 1 ppd, social alcohol PE; ROM hip painfree and full. Normal gait. Guards back – muscle seem to hurt (spasm). **Dull Achilles reflex.** Positive sciatic tension sign. **Decreased sensation lateral border of foot. Weakness**
Posterolateral **HNP (herniated nucleus pulposis)** – L5-S1 with extruded fragment compressing S1 nerve root Treatment plan; NSAIDs, rest (a day or 2 and then get them going), then PT, **epidural steroid injections**, then discectomy (remove the disc)
324
what causes disc herniation (3)
1) **extruded (translig) or sequestered nuclus pulposis** – inflammation (cytokines, macrophages, release of substance P, pain mediated by sinuvertebral nerve). 2) **Bulging annulus fibrosus** (contained herniation). **3) Radiculitis;** inflammation of nerve root
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Case 2.2 **CC; hand numbness for 6 months** HPI; 32 y.o Female 2 year h/o progressively worsening bilateral hand numbness and tingling **predominantly affecting tumb, index, long fingers.** Symptoms **worse at night with prolonged activity** PE; **compression test** - number and tingling at 30 seconds at transverse carpel ligament.
**Carpal tunnel syndrome (median nerve)** Treatment; Night splints (prevent flexing wrist), steroid injections, carpal tunnel release Basic science; Nerve conduction velocity ( EMG show 30 reduction in velocity)
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Case 2.3 CC; **Right shoulder pain** HPI**; 50 y.o** sudden pain **after lifting barbell overhead 2 months ago**. Didn’t get better. Sharp, moderate – severe pain that radiates down the arm. **Worse with overhead activity.** No constitutional signs (fever, chills, unexplained weight loss) PE; No shoulder swelling. **Positive drop arm test.** Weak supraspinatus. **Positive hawkin test for pain** (pinching of bursa of **supraspinatus**)
**Rotator cuff tear - supraspinatous tear** Further workup; Xray – high riding humeral head (rotator cuff tear). **MRI – discontinuity of tendon (rotator cuff tear)** Treatment plan; PT, NSAID, repair the tendons (arthroscopically or open)
327
Cass 3.1 CC; **Right groin pain** HPI; **69 yo female** c/o groin pain for **6 weeks**. Fell and xrays negative. Harder to use walker . **Now severe, sharp nonradiating groin paon, worse with weight bearing** PSH; **smoking**, drinking **(6 beers a day)** PE; **Limps** into office with walker. **R leg shorter than left**. ROM painful. 4/5 strength Xray; irregular contour of the right hip
Missed **femoral fracture Grade IV**. Treated with **Hemiarthroplasty**
328
1. what artery supplies femoral neck 2. treatment of osteoporosis 3. tx of avascular necrosis 4. tx of osteomalacia
1. **_femoral neck (supplies_** (**lateral ascending branch of the medial circumflex artery)** **2.** **_Osteoporosis – bisphosphonate_**, Vit D, pulsatile PTH (forteo). 3. **Avascular necrosis** - if **uncollapsed - core decompression** (stimulate new angiogenesis in the area), if **collapsed treat like osteoporosis (bisphosphanate)** **4. Osteomalacia; find the source. Mostly vit D deficiency – give vitamin D supplement (Know Vit D pathway)**
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Case 3.2 \*\*Identify condition treatmnet CC; Tibia and wrist pain (warm, numbness, road rash and brusing HPI; **14 yo male** in ATV vs truck crash. Swollen left wrist and unstable left shin. NO LOC Questions Differential diagnosis; Closed mid shaft tibia fracture, closed displaced Salter Harris Grade II fracture (involves growth plate and metaphysis) \*\*Later developed pain out of proportion
1. Closed mid shaft tibia fracture; closed reduction and **CAST.** Cast heals by endochondrial ossification (chondrocytes lay down cartilage, osteoclasts absorb the cartilage, osteoblasts lay down new osteoid) 2. Closed Salter Harris Grade II; **CAST** **3.** Compartment syndrome; 5 Ps of compartment syndrome; **_Pain (out of proportion with passive stretch)_**, paresthesia, pulseless, pallor, pokilothermia. There are 4 compartments in the leg. Compartment pressure above 30mmHg is bad.
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Case 4.1 CC; Left thigh pain HPI; 11 mo old infant – painful left thigh with gross deformity. “Fell off a couch” PE; Acute distress. Left thigh swollen with obvious deformity and movement. History; mom stays at home, dad is construction worker. Mom and dad positive for alcohol. Unwitnessed fall. Xray; **Mid-shaft spiral fracture of femur** (spiral fractures are low energy).
**OSTEOGENESIS IMPERFECTA TYPE I** Treatment and test; **Bisphosphate** (do skin biopsy to test collagen)
331
Identify condition - negative birefringement, tophi, hot big toe 1. result in what in blood? 2. Risk per gender? common per what gender? \*\*What is origin of uric acid in man ? (what metabolism?)
1. **_Gout_** is the **result of increased uric acid in the blood (hyperuricemia)**. The higher the **urate level above 6-7 mg/dl** serum, the **greater the likelihood of an attack** of gout occurring. Above this level, uric acid exceeds its solubility at pH 7.4 and **deposits in and around joints** to initiate an attack of gout. **(acute arthritis)** 2. Although the **risk is equal in men and women** at equal serum levels, **more men have hyperuricemia** than women. Therefore, the disease is more commonly seen in men. In **women, gout is most common postmenopausal**. 3. Origin of uric acid; **Purine metabolism**
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Identify causes of gout 1. what idiopathic factors; retention of what? weight? lipi levels? increase production of ? 2. Specific renal retention; what drugs do this? metabolic factors? 3. Nucleic acid turnover ? 4. enzyme defects; increase and decrease of what enzymes 5. local factors; temperature? pH?
**1. Idiopathic** Renal retention of urate Unexplained associations (hypertension, obesity, hyperlipidemia) Increased urate production **2. Renal retention, specific** Drug effects (diuretics, acetylsalicylic acid [aspirin]) Renal damage (glomerular or tubular) Metabolic (lactate, β-OH butyrate) **3. Increased nucleic acid turnover (polycythemias, myeloproliferative disorders, and so forth)** **4. Specific enzyme defects** ↓ Hypoxanthine-guanine phosphoribosyl transferase ↑ Phosphoribosylpyrophosphate synthetase **5. Local factors** Local decrease in urate solubility Low temperature Low pH Possible tissue factors Possible local increase in urate concentration
333
How does gout elicit an inflammatory response to become acute arthritis \*\*what 3 things occur if left untreated?
When **crystals of urate deposit in and around joints**, **granulocytes infiltrate** the area and **phagocytize the crystals**. **Inflammation** ensues with the **release of kinins and lysosomal enzymes** from granulocytes, **↑ lactic acid production to ↓ local pH and ↑ urate deposition,** and release of **chemotaxic factors** to attract more granulocytes to the area. The **cycle continues resulting in pain, swelling of the joint and tenderness.** \*\*\***Untreated,** **_chronic gouty arthritis_, _nephritis_ and _premature sclerosis of blood vessels_** can occur.
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Excretion of urate 1. primary excretion site? 2. how much urate if filtered by glomerulus? 3. is urate actively absorbed? 4. active secretion of urate occurs where? 5. actuve reabsorbtion? 6. how much urate is excreted by urine?
1. Urate excreted **primarily via kidneys** (60-75%). 2. Essentially all urate **filtrated at the glomerulus (~ 100%).** 3. Most urate **actively _reabsorbed_ in _early_ proximal tubule** (S1 segment) (98-100%) 4. **Active _secretion_ of urate occurs in _mid-section_ of proximal tubule** (S2 segment) (~ 50% of reabsorbed urate). _**Inhibition** of secretion by **weak acids** occurs here and results in urate retention._ 5. **Active _reabsorption_ then occurs in _late_ proximal tubule** (S3 segment) and/or distal tubule (~ 80% of secreted urate). 6. Approximately **10% of urate initially filtered at the glomerulus ends up excreted in urine**
335
Identify 3 non-drug therapy of gout - weight? - water? - alcohol
a. avoid obesity - foods high in purine content b. avoid dehydration → ↑ [UA] serum → urate crystal formation c. avoid alcohol → (↓ ADH) → ↑ [UA] serum metabolism to lactic acid → ↓ pH
336
identify Drug therapy of gout 1. antimitotis, anti-inflammatory properties (identify all 5) therapeutic uses a. **treat acute attacks** of gout - a drug of choice (along with NSAIDs) b. **prophylactic usage** to prevent acute attacks of gout in patients with frequent reoccurring attacks of gout. \*\*idnetify toxicity and ways this drug works
**COLCHICINE** a. **↓ leukocyte mobilization** - colchicine binds to microtubular protein and interferes with microtubule function to inhibit mobilization of leukocytes. b. **↓ lactic acid** **production,** ↓ release of lysosomal enzymes from leukocytes c. **↓ release of histamine** from mast cells d. **↓ release of inflammatory glycoprotein** from neutrophils following phagocytosis of urate crystals e. **inhibition of leukotriene synthesis** via inhibition of lipoxygenase pathway. 2. toxicity - **prirmarily GI disturbance (nausea, vomiting diarrhea).** \*\*\*Chronic use - ↑ risk of aplastic anemia, agranulocytosis, myopathy and alopecia.
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Identify drug therapy of gout - an antimetabolite of hypoxanthine which inhibits the enzyme xanthine oxidase to UA formation. - preferred in patients with impaired renal function or a history of renal urate stones - often combined with antineoplastic agents to prevent hyperuricemia. \*\*Identify toxicity and usage \*\*what happens when you fist start this drug? (what 2 drugs prevent this)
**ALLOPURINOL** (Zyloprim) toxicity - uncommon. rash, fever, vasculitis, hepatotoxicity, bone marrow toxicity. therapeutic uses * *a. chronic gout b. secondary hyperuricemia** **When allopurinol therapy is started**, an **_acute attack of gout_** may be precipitated due to **fluctuations in serum urate levels** and the resulting dissolving of deposited urate crystals. **Colchicine or a non-steroidal antiinflammatory** can be used to **prevent the symptoms of an acute gout attack.**
338
identify drug of gout therapy - another xanthine oxidase inhibitor (first is allupirinol) - A non-purine drug that forms a stable complex with xanthine oxidase (reduced or oxidized form) and inhibits enzyme activity in either state. b. Pharmacokinetics-absorption reduced by magnesium hydroxide and aluminum hydroxide antacids. Absorption slightly reduced by food. \*\*identify use and toxicity
Febuxostat (Uloric) Febuxostat is approved for use in hyperuric patients with gout attacks, but is not recommended for patients with asymptomatic hyperuricemia. d. Toxicity- liver function abnormalities, nausea, joint pain and rash. e. As with allopurinol, initiation of febuxostat therapy may cause an acute attack of gout due to decreased serum levels of urate which mobilizes urate from deposited crystals. Concurrent NSAIDs or colchicine therapy is usually required when febuxostat therapy is started. Maybe an increased rate of myocardial infarction or stroke; causal relationship to drug use not fully established.
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identify gout drug therapy Recombinant urate oxidase enzyme that catalyzes the oxidation of uric acid into soluble allantoin. Lowers uric acid plasma levels better than allopurinol. 2. Indications –initial treatment of elevated plasma urate levels in pediatric patients with leukemia, lymphoma and solid tumors who are receiving cancer chemotherapy treatments that will result in cell lysis and hyperuricemia. 3. Efficacy can be reduced by antibody production against the enzyme in treated patients \*\*\*\*Indentify toxicity\*\*
**Rasburicase (Elitek)** Toxicity-**hemolysis in GGPD deficient patients**, **methemoglobinemia**, acute renal failure and anaphylaxis have been observed.
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Gout drug - uricosuric agents (2) - Mechanism of action - Competitively inhibit active reabsorption of urate by primarily URAT-1 in the proximal tubule of the nephron to increase urate excretion. Low doses only inhibit active secretion (a more sensitive system) of urate to cause UA retention. Therapeutic uses a. **chronic gout b. hyperuricemic states** c. sulfinpyrazone has been shown to ↓ platelet aggregation and is an experimental agent in the prophylactic treatment of myocardial infarctions.
Uricosuric Agents - **Probenecid (Benemid) and Sulfinpyrazone (Anturane)** Toxicity - GI irritation with aggravation of peptic ulcer (sulfinpyrazone \> probenecid) 3. **Uricosuric agents increase the UA concentration in urine by inhibiting reabsorption. T**o minimize intrarenal urate stone formation, fluid intake should be ↑ and the urine can be alkalinized (bicarbonate) when initiating therapy. 4. Although less frequently than allopurinol, **uricosuric agents may precipitate an acute attack of gout** and colchicine or an NSAID may be used prophylactically when initiating therapy.
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identify gout drug **increases urate excretion without urate retention**. May be used in patients with **decreased renal function or patients allergic to probenecid or sulfinpyrazone**. In use in Europe.
**Benzbromarone (Exurate)**
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Identify 2 extra drugs for gout \*\*Both anti-inflammatory agents
1. **Non-steroidal antiinflammatory agents (NSAIDs) –NSAIDs, including selective COX-2 inhibitors,** can be effective to ↓ inflammation (except acetaminophen) and reduce pain in acute attacks of gout. Although NSAIDs are effective, indomethacin, naproxen and sulindac are the only FDA- approved NSAIDs to treat acute attacks of gout .Aspirin should be avoided in gout patients because at normal doses, aspirin ↓ urate secretion and at high doses aspirin ↑the risk of renal calculi. In acute attacks of gout, NSAIDS or glucocorticoids may be preferred to colchicine in elderly patients with cardiac, renal or GI diseases. 2. **Glucocortiods (e.s. prednisone)** - used for acute gout when other conventional therapies fail to control an acute attack or in elderly patients where colchicine should be avoided.