Ex 1 Wk 2 ORTHO

Question 1

Role of orthopaedic surgery

• definition
• meaning
• timeline

Answer 1

• 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

Question 2

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)

Answer 2

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

Question 3

Most important diagnostic test in orthopaedics

why ?

Answer 3

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

Question 4

1. what can you see on X-ray?

**2 classes (3 each)

Answer 4

•Radio-opaque items

–Bones

–Some soft tissues

–Hardware

•Radio-lucent items

–Air

–Sutures

–Ligaments

Question 5

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?

Answer 5

• 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?

Question 6

Describe the fracture

Answer 6

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

Question 7

Trama evalation

ABCs

Answer 7

• 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

Question 8

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

Answer 8

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

Question 9

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?

Answer 9

• 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

Question 10

Routine xrays

**what is recommended with hip dislocation or acetabular fracture

Answer 10

• 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.

Question 11

Upper extremity exam (4)

Answer 11

• 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)

Question 12

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

Answer 12

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!

Question 13

Exam of upper extremity

Brachial plexus

pre vs post ganglionic

Answer 13

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

Question 14

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

Answer 14

Pelvis

Question 15

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

Answer 15

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

Question 16

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?

Answer 16

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

Question 17

Vasculature of lower extremity

**Hip vs knee dislocation

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

Answer 17

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

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

Question 18

Systemic approach to reading plain radiograph (5)

Answer 18

• 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

Question 19

facts of child absue

• age
• common fractres

Answer 19

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)

Question 20

differential dx of child with fracture (4)

Answer 20

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

Question 21

child with a fracture

**Not usually abuse (5)

Answer 21

• 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

Question 22

• 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

Answer 22

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….”

Question 23

Definitions

1. fractured bone
2. comminuted
3. Non-union
4. Osteomyelitis
5. Neurovasclar injury
6. compound fracture (old terminology)

Answer 23

• 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

Question 24

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.

2. compromise or loss of perfusion distal to the site of injury – pulses + capillary refill vs. CR only vs. cold ecchymotic limb

Answer 24

1. Open Fracture
2. Vasclar injury

Question 25

Definition

ORIF

Ex-fix

Reduction

CR

NV

IMN

Answer 25

• 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

Question 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

Answer 26

1. Intraarticular fracture
2. Long bone

Question 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?? ****

Answer 27

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

Question 28

Emergencies; life or limb

**give examples of absolute (5) vs relative emergencies (4)

**when can a relative emergency become an absolute emergency

Answer 28

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)

Question 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

Answer 29

URGENCY - not emergency

**Patient has a FALL

Question 30

treatments

1. what you need for every open fracture
2. when fecal matter is involved
3. compartment syndrome?

Answer 30

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

Question 31

5 P’s of Ischemia

**What is most important P in compartmnet syndrome?

Answer 31

• Pain
• Palor
• Parasthesia
• Pulse (less)
• Poikilothermia

**Pain is the most important in compartment syndrome, then dysthesia – the others tend to be late findings

Question 32

4 C’s of muscle viability

**What fractures get surgery

Answer 32

• 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)

Question 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

Answer 33

SCAPULA

Question 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?

Answer 34

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)

Question 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?)

Answer 35

HUMERUS

• Fracture brace early
• ORIF only if polytrauma, displaced, non-union and certain cases neurovascular compromise
• Early shoulder motion

Question 36

UE - Forearm

**Identify risks (2), temporization and definitive care (2)

Answer 36

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

•

Question 37

LE; Pelvis/acetabulum

• marker for?
• identify risks, temporization and definitive care?

Answer 37

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

Question 38

identify condition **

**What is the treatment

Answer 38

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

Question 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

Answer 39

FEMUR

**Marker for high energy marker in extremities - Scapula, pelvis/acetabulum and femur

Question 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

Answer 40

TIBIA/FIBULA

Question 41

LOW ENERGY MECHANISM

• arise from what in elderly?
• types of fractures (6)
• what is a pathologic condition?

Answer 41

•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!!!

Question 42

Anatomy of hand

• identify 3 joints in hand
• 1 joint in feet

Answer 42

1. Hand joint
   - Distal interphalangeal joint (DIP)
   - Proximal interphalangeal joint (PIP)
   - Metacarpal phalangeal joint (MCP)
2. Foor joint

Foot MTP: Metatarsal phalangeal joint

Question 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

Answer 43

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

Question 44

osteoarthritis

• condition
• phases

Answer 44

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

Question 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?

Answer 45

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

Question 46

Areas affected in osteoarthritis (7)

Areas spared (3)

**remember that osteoarthritis is a degenrative joint disease so we talking about joints here

Answer 46

OSTEOARTHRITIS

Areas affected; Hips, Knees, Lower lumbar, Cervical, DIP, PIP, First Carpometacarpal joints

SPARES: wrists, elbows, shoulders joints

Question 47

Identify condition in picture

Answer 47

Osteophytes - bone spore (Osteroarthritis)

*can be in DIP joint in women - called Heberden’s Nodes

Question 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?

Answer 48

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

Question 49

pathogenesis of rheumatoud arthritis

• 2 types of antibodies foremd (which is specific? non-specific?)
• 2 components of synovial fluid (high vs low)

Answer 49

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

Question 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?

Answer 50

RHEUMATOID ARTHRITIS

Question 51

identify joint condition

**Flexion-hyperextension of fingers (swan neck; boutonniere)

-other presentations on xray (3)? 3 others

Answer 51

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)

Question 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)

Answer 52

Rheumatoid nodules

Question 53

what condition that occur in rheumatoid arthristis affect blood vessels

Answer 53

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

Question 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)

Answer 54

JUVENILE IDIOPATHIC ARTHRITIS

Extra-articular manifestations: pericarditis, myocarditis, pulmonary fibrosis, uveitis, glomerulonephritis, growth retardation

Question 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

Answer 55

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

Question 56

Identify joint condition

• Pathology in ligamentous attachments Immune mediated; no specific autoantibody
• Many are + HLA B27

Rheumatoid factor NEGATIVE

**4 examples

Answer 56

Seronegative Spondyloarthropathies

1. Ankylosing spondyloarthritis
2. Enteritis-associated arthritis (IBD)
3. Reactive arthritis (reiter’s)
4. Psoriatic arthritis

***PAIR ACRONYM

Question 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

Answer 57

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

Question 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?

Answer 58

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

•

Question 59

identify extra-articular problems with reiter syndrome

Answer 59

Extra-articular

• Balanitis
• Conjunctivitis
• Heart conduction defects
• Aortic regurgitation
• Symptoms wax and wane with 50% recurrence

Question 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

Answer 60

ENTERITIS-ASSOCIATED ARTHRITIS

Question 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

Answer 61

PSORATIC ARTHRITIS

**10% in psoriasis patients

Question 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?)

Answer 62

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

Question 63

conditions with infectious arthritis (3)

***Where do you see Borrellia burgdofreri (cockscrew image)?

Answer 63

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

Question 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

Answer 64

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

Question 65

Gout

• what precipitates?
• is it an arthritis?

**What 3 things indicate gout?

Answer 65

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)

Question 66

Identfiy gout phases (4)

Answer 66

• Asymptomatic hyperuricemia
• Acute arthritis; 50% First MTP joint foot. Instep > ankles > heels > knees > wrists
• Intercritical gout: No symptoms
• Chronic tophaceous gout

Question 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

Answer 67

TOPHI

Question 68

Risk factos of gout (6)

Answer 68

• > 30 years (ie duration of hyperuricemia)
• Genetic predisposition
• Heavy drinking
• Obesity
• Drugs eg thiazides
• Pb toxicity

Question 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

Answer 69

CALCIUM PYROPHOSPHATE CRYSTAL DEPOSITION DISEASE (CPPD)

Question 70

• < 2 cm cyst near joint or tendon sheath
• Wrist is most common
• Cystic or myxoid degeneration of tissue
• No communication with joint space

Answer 70

Ganglion Cyst

Question 71

identify

•Connected to a joint capsule or bursa

• cyst often in setting of Rheumatoid Arthritis

Answer 71

Synovial cyst

Question 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

Answer 72

TENOSYNOVIAL GIANT-CELL TUMOR

Question 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

Answer 73

DIFFUSE TENOSYNOVIAL GIANT-CELL TUMOR

**hard to get rid off. usually reoccur

**Shag carpet villi

Question 74

• Well circumscribed
• Often attached to synovium or tendon
• Slow growing painless
• Fingers and wrists (Most common soft tissue tumor of hand; especially fingers)

Answer 74

LOCALIZED TENOSYNOVIAL GIANT-CELL TUMOR

**soft tissue mass in finger

Question 75

Give examples of soft tissue tumors

Answer 75

• Fatty (Adipose tissue)
• Fibrous
• Fibrohistiocytic
• Skeletal muscle
• Smooth muscle
• Vascular
• Peripheral nerve
• Tumors of uncertain histogenesis

Question 76

General principles of soft tissue tumors

• which is more in numer (benign or malignant?)
• metastasis
• what parts of body?
• most common cause?
• Associations

Answer 76

• 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

Question 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

Answer 77

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

Question 78

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

Answer 78

Picture

Question 79

What type of tumor is this?

Answer 79

Tumor that big is Sarcoma (soft tissue)

**Soft tissue sarcoma - barely touching bone, color variation

Question 80

General principles of soft tissue sarcoma

• most common in children vs adults

Answer 80

• 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

Question 81

Prognosis of sarcoma

**3 things affect prognosis

Answer 81

1. Type (recapitulation of tissue type)
2. Stage (location and size)

•Superficial vs deep, size, metastasis, etc

3. Grade

• Cell pleomorphism
• Necrosis
• Mitotic rate

Question 82

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?

Answer 82

Table

Question 83

**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)

Answer 83

Table

Question 84

identify 2 fatty tumors

Answer 84

1. Lipoma
2. Liposarcoma

Question 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

Answer 85

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

Question 86

Identify fatty tumor

A, Adults 40-60

B. Deep soft tissues

• Retroperitoneum (often very large)
• Proximal extremities

C. Types (4)

Answer 86

LIPOSARCOMA

**In retroperitonium

4 types

• Well-differentiated (retroperitoneal)
• Myxoid/Round cell (extremities)
• Pleomorphic-very aggressive course
• Dedifferentiated

Question 87

Most common type of liposarcoma

**what mutation is amplified?

**what mutation is inhibited?

Answer 87

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)

Question 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

Answer 88

Liposarcoma, myxoid/round cell

**Chicken wire capillaries (thin vessels). Myxoid tend to be indolent

Question 89

Other types of liposarcoma (2)

• very aggresive one
• the other arise from well-differntiated liposarcoma

Answer 89

• Pleomorphic liposarcoma: Very aggressive
• Dedifferentiated liposarcoma: Sarcoma arising from a well-differentiated liposarcoma

Question 90

Types of fibrous (myofibroblastic) tumors/proliferations (4)

Answer 90

1. Benign reactive proliferations

• Nodular Fasciitis
• Myositis Ossificans

2. Fibromatoses

• Deep fibromatosis (Desmoid)
• Superficial Fibromatosis

3. Fibroma
4. Fibrosarcoma

Question 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

Answer 91

Nodular fasciitis

**Type of benign reactive proliferation

Question 92

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

Answer 92

Myositis/Panniculitis Ossificans; second type of benign reactive proliferation. **The first is nodular fasccitis.

**Ossificans refer to bone

Question 93

Radiology:

**Identify tumor type?

**what is a differential that can be mistaken with this?

Answer 93

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

Question 94

2 types of fibromatoses

Answer 94

1. Superficial Fibromatosis

• Palmer Fibromatosis
• Plantar Fibromatosis (nodule on foot)
• Penile Fibromatosis

2. Deep-seated Fibromatosis (Desmoid tumor)

• Extra-abdominal
• Abdominal
• Intra-abdominal

Question 95

• Nodular or poorly defined fascicles of fibroblasts and abundant collagen
• Course: May progress, regress or stabilize
• May recur after excision

Answer 95

Superficial Fibromatosis

Question 96

identify fibrous tumor? (aka what disease)

**is it usually bilateral?

Answer 96

Palmer Fibromatosis (Dupuytren’s contracture)

• Nodular thickening of palmer fascia; puckers skin and digit flexion contraction (mostly 4 and 5)
• 50% bilateral

Question 97

Identify fibrous tumor?

Answer 97

Plantar fibromatosis (superficial firbromatoses)

• Bilateral infrequent
• Irregular of nodular thickening of plantar fascia

Question 98

identify tumor (aka what disease?)

• Induration or mass on dorsolateral penis
• Can cause abnormal curvature of penis
• Can constrict urethra

Answer 98

• *Penile Fibromatosis**
• *(Peyronie’s Disease**)

Question 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

Answer 99

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

Question 100

identify fibrous tumor type

• Gray-white poorly demarcated
• Fibroblasts in fascicles infiltrate tissue

***Types

Answer 100

**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

Question 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?

Answer 101

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

Question 102

Types of skeletal muscle tumors

• which is most common in kids (types?)

Answer 102

1. Rhabdomyoma (rare benign)
2. Cardiac rhabdomyoma (see chapter 12)
3. Rhabdomyosarcoma (most common in kids)

• Embryonal
• Alveolar
• Pleomorphic

Question 103

**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)?

Answer 103

Rhabdomyosarcoma (skeletal muscle tumor)

• Desmin positive (brown color in cytoplasm)
• MyoD1 (muscle transcription factor psitive) - same pattern for myogenin

Question 104

identify tumor type

• 60% of rhabdomyosarcomas
• Children < 10 years
• Subtypes:?? in walls of hollow viscera and mucosal lined structures

Answer 104

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

Question 106

Describe the slides

**components of what tumor type?

myogenin markers positive or negative?

Cross striations positive or negative?

Round blue cells?

Answer 106

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)

Question 107

Identify tumor type

• tranlocation?
• prognosis?
• age range affected?
• body part affected

Answer 107

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.

Question 108

**Identify skeletal muscle tumor type

• age group?
• mistaken for what othe rtumor type?
• myogenn? desmin?

Answer 108

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

Question 109

Prognosis of rhabdomyosarcoma

Answer 109

• Sarcoma botryoides: Best
• Embryonal: Second best
• Alveolar and Pleomorphic: Poor
• 65% of children are cured
• Adults do poorly

Question 110

•Benign smooth muscle tumor

•Most common in uterus (chapter 22)

Age group?

*****other sites?

• component of the slide?
• rare in what body part

Answer 110

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

Question 111

Identify soft tissue tumor

**contents ?

what is present vs absent? (myogenin? myoD1, actin? desmin?)

Answer 111

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

Question 112

**identify soft tissue tumor

• tranlocation and fusin gene
• cell type ***what is UNIQUE about this?
• Classic location?***

Answer 112

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

Question 113

2 types/variants of synovial sarcoma

**Do they both stain positive for cytokeratins?

Answer 113

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)

Question 114

• Group of aggressive neoplasms
• Diagnosis of exclusion
• Proximal extremities and retroperitoneum
• Large grey, hemorrhagic and/or necrotic
• Metastasis 30-50%

**Identify cell pattern

Answer 114

Undifferentiated Pleomorphic Sarcoma (Malignant Fibrous Histiocytoma)

•**Cell pleomorphism and storiform pattern

Question 115

Immunohistochemistry of soft tissue tumors

• which is specific for skeletal muscle?
• smooth muscle?
• non epithilial tumor?

Answer 115

• 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

Question 116

Summary list of soft tissue tumors

Spindle cells; give examples of beign and malignant tumors in the following

• myofibroblastic
• smooth muscle
• unknown

Answer 116

Question 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

Answer 117

Question 118

What soft tissue tumor is biphasic ??

**is it benign or malignant?

Answer 118

SYNOVIAL SARCOMA

**malignant

Question 119

Identify painful skin lesions “Blue ANGEL” (6)

Answer 119

• BLUE rubber bleb nevus
• Angiolipoma
• Neuroma (traumatic)
• Glomus tumor
• Eccrine spiradenoma
• Leiomyoma (cutaneous)

Question 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?

Answer 120

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

Question 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

Answer 121

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

Question 122

treatment options for osteoarthritis (10)

Answer 122

–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 Replacement (most successful in hip and knee and shoulder). Risk for dislocation, infection, stiffness. Longevity 10-20 years.

Question 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

Answer 123

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.

Question 124

Exam, tests and X-rays of rheumatoid arthritis

Answer 124

•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)

Question 125

Treatment options for rheumatoid arthritis

Answer 125

•Treatment

–NSAIDs

–Steroids

–DMARDs; Hydroxychloroquine, methotrexate, gold, Embrel

–Surgery

Question 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

Answer 126

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

Question 127

Identify common bugs that cause septic arthritis in the following

1. neonate
2. <5y.o
3. >5y.o to <teens></teens>

<p>4. adolescents </p>

<p>5. adults </p>

<p>6. Sickle cell patients </p>

<p>7. Chronic picture </p>

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

</teens>

Answer 127

–Neonate = Staph Aureus, Group B Strep

–<5yo = Staph Aureus, group A strep, H flu, strep pneun

–>5 to <teens></teens>

<p><strong>–Adolescents = Gonorrheoeae</strong></p>

<p>–Adults = Staph Aureus</p>

<p>–Sickle Cell Patients = Salmonella</p>

<p>–Chronic Picture = TB or Lyme</p>

<p>**</p>

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

<p>-In sexually active patients esp adolescents, most common bug is GONORRHEA</p>

</teens>

Question 128

treatment for septic arthritis (2)

Answer 128

–Surgical washout

–Antibiotics

Question 129

4 types of seronegative spondyloarthropathies

Answer 129

1. Ankylosing spondylitis
2. Reiter disease
3. Psoriatic arthritis
4. IBD

Question 130

Identify type of seronegative spondyloarthropathy - ankylosing spondylitis

• frequency?
• what happens to joints?
• 2 charateristic features (labs)
• 3 presentations/conditions

Answer 130

•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)

Question 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

Answer 131

REITER DISEASE

Question 132

Identify types of seronegative spondyloarthropathy

–Nail disorders

–Iritis

Answer 132

Psoriatic arthritis

–5-10% of those with psoriasis

Question 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

Answer 133

IBD (inflammatory bowel disease)

Question 134

Seronegative spondyloarthropathy

• symptoms
• exam
• labs
• treatment

Answer 134

•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

Question 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?

Answer 136

1. End of day
2. 1 in 2000 persons
3. C1-2 instability

Question 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?

Answer 137

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.

Question 138

MSK tumors

• tumors come from where?
• cancers called? frequency?
• metastasize to what organ?

Answer 138

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

Question 139

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

Answer 139

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

Question 140

MSK tumors

1. History (4)
2. Physical exam (4)

Answer 140

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

Question 141

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

Answer 141

–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?

–

Question 142

MSK tumors

1.

• what happens over age 40?
• growing soft tissue masses are?
  2. treatment of MSK tumors

Answer 142

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)

Question 143

Identify treatment of MSK tumors

1. Ewing/PNET
2. Osteosarcoma
3. Chondrosarcoma

Answer 143

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)

Question 144

MSK tumors - age and histopath

1. Ostosarcoma
2. Ewings/PNET
3. Chondrosarcoma
4. metastatic disease

Answer 144

Osteosarcoma; 1^st decade, swelling and night pain, HIstopatho – Pink plus osteoblasts (thick osteosarcoma) with football shaped cell.

Ewings/PNET; 2^nd 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

Question 145

Identify condition - Osteomyelitis

1. what happens to bone? what part of bone is preferred?
2. Most common bacteria?
3. How is it spread?

Answer 145

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.

Question 146

History and exam of osteomyelitis

**do you have pain with ROM ?? (as opposed to what joint condition?)

Answer 146

•History:

–Achy, unrelenting night pain

–Fever

•Exam:

–Tenderness in bone

–ROM of joints is ok; Unlike in septic arthritis

–Swelling, warmth, redness, draining sinus

Question 147

Osteomyelitis - tests

**What is the gold standard for diagnosis

**Identify other tests and why order them (5)

Answer 147

–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

Question 148

Treatment of osteomyelitis

Answer 148

•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

Question 149

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.

Answer 149

Osteoporosis

Question 150

2 types/forms of osteoporosis

• which has type I and II (describe them)

Answer 150

•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

Question 151

History and exam of osteoporosis

Answer 151

•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

Question 152

What tests to detect osteoporsis and why order them

Answer 152

•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

Question 153

identify prevention and treatment of osteoporsis

Answer 153

•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)

Question 154

• 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.

Answer 154

• 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

Question 155

• 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”?

Answer 155

• 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

Question 156

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)

Answer 156

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)

Question 157

Identify condition in sports - idiopathic loss of shoulder motion

- associated with what systemic disease?

• symptoms (2)
• exam (2)
• tests
• treatemnt

Answer 157

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?

Question 158

Identify sports condition - Inflammation of subacromial bursa and rotator cuff tendons in middle aged persons

• symptoms
• exam
• tests
• treatment

Answer 158

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

Question 159

Identify sports condition

•Degenerative painful condition of the ECRB (lateral) tendon and / or flexor-pronators (medial)

• symptoms
• exam

tests

treatment

Answer 159

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

Question 160

Identify sports condition

**Indicate test and treatment (what is diagnostic?)

• Symptoms
• Locking and catching in the knee
• Exam

•McMurrays +

•Joint line tenderness

Answer 160

Menisci tear; Fraying or tear of menisci

• Tests
• Xrays negative
• MRI shows tear – diagnostic
• Treatment
• PT
• Arthroscopic debridement
• BS
• Anatomy of knee

Question 161

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

Answer 161

Olecranon Bursitis - inflammation of olecranon bursa

**associated with Gout

Question 162

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

Answer 162

Patellofemoral pain - Pain around the patella without signs of arthritis, common in teenagers during growth spurt

Question 163

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

Answer 163

Plantar Fasciitis - Degenerative tear of plantar fascia, more common in women and overweight persons with tight gastroc-soleus tendons

Question 164

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)

Answer 164

Rotator cuff tear - Tear of supraspinatous (most common), infraspinatous, subscapularis, or teres minor.

•Acutely in young, chronic degeneration in older.

Question 165

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.

Answer 165

Rupture of proximal biceps tendon; •Rupture of long head of biceps, with labral injury

Question 166

• 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

Answer 166

Trochanteric bursitis - Inflammation of greater trochanteric bursa from tight IT band

Question 167

• 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?

Answer 167

• 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

Question 168

1. 3 bones that attach to knee
2. suppoting stuctues of the knee

Answer 168

1. Femur, tibia, fibula
2. capsule, ligaments, minisci, muscle

Question 169

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?

Answer 169

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

Question 170

identify types of graft used to reconstruct ACL

Answer 170

Question 171

Advantages and diasvantages of BTB autograft used in ACL reconstruction

Answer 171

Question 172

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?

Answer 172

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.

Question 173

identify condition

• mostly anterior dislocation (basketballer)
• GH joint has largest ROM in body
• poor articular conformity

Answer 173

ANTERIOR SHOULDER DISLOCATION

Question 174

Identify body part

**Loss reduces force to dislocate 50%

• triangular rim of fibrocartilaginuous tissue; extension of bony glenoid.

Answer 174

LABRUM
Attachment sites; GH ligaments, capsule, biceps

Question 175

Epidemiology of labrum tear (lead to anterior shoulder dislocation)

• age with higher probability of another dislocation (based on age)

Answer 175

• probability 50% of re-dislocation in men at 27 years and women at 17 years old.

**Arthroscopic labral repair - helps

Question 176

Identify

• most common sports-related injury (up to 50% of all sports injuries); basketball injuries and even pro golfers
• NOT A BENIGN INJURY

-

Answer 176

“Low” Ankle Sprain

Question 177

Tests of lateral ankle sprain exam (2)

Answer 177

1. Anterior drawer
2. Tala tilt

Question 178

Grades/severity of ankle sprain (injury, swelling, weight bearing)

Answer 178

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

Question 179

How to treat ankle sprain

(3)

**another one does not treat but prevent recurrence

**when do you need surgery

Answer 179

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

Question 180

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

Answer 180

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

Question 181

Skeletal muscle - definitions

• tonic spasms
• deficeint ton e
• fixation joints
• high enzyme in muscle and brain

Answer 181

• 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

Question 182

*****Identify sign - skeletal muscle

• indicates weakness of the proximal muscles
• Uses the hands and arms to “walk” up from a squatting position

Answer 182

GOWER’S SIGN

Question 183

**Picture of I and A band

• which is light vs dark band
• During contraction; which shortens and which remains unchanged?

Answer 183

Picture

Contraction: I band shortens (LIGHT COLOR); A band is unchanged (DARK COLOR)

Question 184

Differences in type 1 vs type 2 based on fiber type

• action type
• actin
• fibers (slow or fast)
• metabolism

Answer 184

Picture

Question 185

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

Answer 185

• “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

Question 186

Identify condition

• Disorder of motor neurons
• Breakdown of myosin and actin
• Resorption of myofibrils

Answer 186

Denervation Atrophy

Question 187

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)

Answer 187

Spinal Muscular Atrophy (Infantile Motor Neuron Disease; SMA)

Question 188

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

Answer 188

Muscular Dystrophy

**Most common type is DMD

Question 189

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

Answer 189

DMD

Question 190

• 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

Answer 190

DMD

Question 191

identify condition

Answer 191

DMD- Duchenne Muscular Dsytrophy

Question 192

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

Answer 192

Becker MD

Question 193

MD female carrier DMD vs BMD

• dilated cardiomyopathy
• LV dilation by echo
• elevated CK
• Weakness

Answer 193

Picture

**In BMD, no chance of dilated cardiomyopathy

Question 194

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

Answer 194

Limb Girdle Muscular Dystrophy

Question 195

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

Answer 195

Facioscapulohumeral MD

Question 196

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

Answer 196

Emery-Dreifuss MD

Question 197

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

Answer 197

Myotonic dystrophy

Question 198

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

Answer 198

Myotonic Dystrophy

***Many CTG repeats expansion on 19q

**Anticipation

**Characteristic face - drooping, gaping mouth, arthrophy, myotonia, christmass tree cataract

Question 199

identify skeletal condition

• Familial
• Myotonia and/or hypotonic paralysis
• Malignant hyperpyrexia

Answer 199

Ion Channel myopathy ; Channelopathies” mutations in ion channels

**Most common is hypokalemic periodic paralysis

Question 200

Types of hypotonic channelopathies (3)

Answer 200

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

Question 201

identify channelopathy

• complication from surgery (from anesthesia)
• very high fever, tachypnea, muscles completely contrat (over heating will then happen)

Answer 201

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

Question 202

Identify condition

• Release Ca++ from sarcoplasmic reticulum
• ATP is depleted by muscle contraction
• Anaerobic metabolism: Lactic acidosis
• Hyperthermia
• Rhabdomyolysis
• Hyperkalemia
• Renal failure

•Treatment: Dantrolene

Answer 202

Malignant Hyperthermia/Hyperpyrexia

Question 203

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

Answer 203

Congenital Myopathy

Question 204

• Autosomal dominant
• Hypotonia
• Ryanodine receptor -1 (RYR1) gene defect
• Risk for malignant hyperthermia
• Centrally light area in type 1 fibers

Answer 204

Central core disease

Question 205

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

Answer 205

Nemaline myopathy

Question 206

A. Various types (3)

• X-linked
• Autosomal dominant
• Autosomal recessive:

B. Central nuclei usually confined to type 1 fibers

Answer 206

Centronuclear (myotubular) Myopathy

Question 207

• Accumulate lipid in myocytes
• Defects in carnitine transport system
• Defects in mitochondrial dehydrogenase enzyme system

Answer 207

Lipid myopathy

Question 208

• 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

Answer 208

Mitochondrial myopathy

**Kmart

Question 209

Identify picture

***RED RAG FIBERS

Answer 209

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.

Question 210

Inflammatory myopathies

1. infectious e.g
2. Noninfectious (3)
3. systemic inflammatory disease (2)

Answer 210

1. Infectious

•Trichinella spiralis

2. Noninfectious

• Dermatomyositis
• Polymyositis
• Inclusion Body Myositis

3. Systemic Inflammatory Diseases

• Systemic Sclerosis (Scleroderma)
• Sarcoidosis

Question 211

***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

Answer 211

Dermatomyositis

**Perimysium affected

Question 212

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

Answer 212

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.

Question 213

Picture - non infectious inflammatory myopathy

**Talengentasias of nails

**Rash

**myalgia

Answer 213

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)

Question 214

• 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

Answer 214

Polymyositis; no rash, endmysium

Question 215

**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

Answer 215

Inclusion Body Myositis

Question 216

Differences in inflammatory myopathies

3 types

• lymphocytes
• respond to immunosuppresant
• injury site
• begins (proximal or distal)
• CK

Answer 216

Picture

Diagnosis depends on

Clinical symptoms

↑ Creatinine Kinase (CK)

EMG: Mixed myopathy and neuropathic findings

Biopsy

Question 217

Toxic myopathies (3)

Answer 217

• Thyrotoxic
• Ethanol
• Drug induced

Question 218

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

Answer 218

Thyrotoxic myopathy

Question 219

type of myopathy

• Cramping/aching muscle; slow movements
• Slow reflexes
• Proximal weakness eg posterior neck
• Elevated CK
• Fiber atrophy

Answer 219

Hypothyroidism Myopathy

**Head ptosis

Question 220

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

Answer 220

Ethanol Myopathy

Question 221

Durg induced myopathy (3)

Answer 221

•Steroid myopathy

•Proximal weakness: Atrophy of predominately type 2 fibers

•Chloroquine myopathy

• Proximal weakness
• Vacuoles in myocytes

•Statins

•1.5% of users

Question 222

• Profound weakness
• Associated with corticosteroid therapy
• Degraded myosin thick filaments

Answer 222

ICU Myopathy (Myosin deficient myopathy)

Question 223

• Neuromuscular Junction Disease: Immune-mediated loss of acetylcholine receptors
• Circulating Anti AChR
• Decreased AChRs
• Thymic hyperplasia: 30%

•Thymoma (an eptihelial neoplasm): 10%

Answer 223

Myasthenia Gravis

Question 224

**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

Answer 224

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

Question 225

• 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

Answer 225

Lambert-Eaton Myasthenic Syndrome

**graph show it gets rapid

**myasthernia gravis graph - show decline

Question 226

• Name the other structures in the carpal tunnel.
• L5 innervates what part of the foot?
• Radiculopathy is an upper or lower motor neuron phenomenon?

Answer 226

• 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

Question 228

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

Answer 228

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

Question 230

•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

Answer 230

Carpal tunnel syndrome

**compression of median nerve at the wrist

Question 231

what goes through carpal tunnel (4)

Answer 231

Flexor digitorium superficialis

Flexor digitorium profundus

Flexor policis longus

Median nerve

Question 232

•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

Answer 232

Trigger Finger

**•Inflammation of flexor tendon gets it snapping through pulleys in hand.

Question 233

identify condition

Symptom and exam; inability to straighten finger tip

Treatment; Stack splinting

**Test and diagnosis

Answer 233

Mallet finger ; Laceration of extensor tendon at base of the DP

**–Xray may show avulsion fracture at base of DP

Question 234

identify condition

• symptoms; pain over radial styloid
• treatment; Splint, NSAIDs, steroid injection, release of first dorsal compartment

**Diagnosis, condition, exam

Answer 234

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

Question 235

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?

Answer 235

Dupuytren Disease; Nodular thickening of palmar fascia (Northern european descent)

**Fold of palmar fascia. Nodules cause digits to flex down

Question 237

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

Answer 237

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_

Question 238

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

Answer 238

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

Question 239

Describe intervertebral disc structure

**what nerve innverates the disc

Answer 239

What’s missing in this pie chart? Cell! Also mention that it is largely avascular, 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

Question 240

identify lumbosacral dermatones

• what innervates; umbilicus? patella reflex? dorsum of foot? back of foot?

Answer 240

T10 – umbilicus

L4- patella reflex

L5 – dorsum of foot

S1,S2; back of foot (achilles heel)

Question 241

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

Answer 241

Spondylolisthesis; Forward slippage of lumbar vertebral body.

• Tests –Flexion / extension Xrays of spine show slippage
• Treatment –NSAIDs, surgical fusion

Question 242

Identify condition

Answer 242

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)

Question 243

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

Answer 243

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 protect the neural elements and allow for mobility.

Question 244

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

Answer 244

Spondylosis; Degenerative changes in the facets or discs leading to osteophytes and possible nerve compression

***Osteophytes cause foramenal stenosis from facet arthritis

Question 245

identify condition of the spine

Answer 245

Spondylosis

•Degenerative changes in the facets or discs leading to osteophytes and possible nerve compression

Question 246

identify the cervical dermatomes

• ear
• front part of arm
• thumb
• first 2 digits
• last 2 digits

Answer 246

Cervical dermatomes

C2 – ear

C5 – front part of arm

C6 – thumb

C7 – first 2 digits

C8 – last 2 digits

Question 247

Cervical myotomes

from C5 to T1 (identify)

Answer 247

• C5 – Deltoid
• C6 – Biceps, wrist extensors
• C7 – Triceps, wrist flexors
• C8 – Finger flexors
• T1 – Interossei

Question 248

Identify condition

•Symptoms

–Stiff spine, pain

•Exam

–Stiff spine

•Tests

–Xrays show bridging osteophytes over 4 vertebra, no HLA association

•Treatment

–NSAIDs

Answer 248

DISH - Idiopathic disease characterized by osteophyte formation spanning several vertebra

Question 249

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

Answer 249

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.

Question 250

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

Answer 250

Myelopathy; compression of the spinal cord

•Treatment –Epidural injections may help, but surgical decompression is recommended due to risk of permanent deficits

Question 251

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

Answer 251

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)

Question 252

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?

Answer 252

Babesiosis (not travelled outside US)

Treatment; Mild disease: Atovaquone PLUS azithromycin

Vector – Blacklegged tick (Ixodes scapularis) in eastern US.

Question 253

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

Answer 253

RMSF (Rocky mountain Spotted Fever) - Rickettsia rickettsii

treat with DOXYCYCLINE.

RMSF; caused by rocky mountain wood tick (dermacentor andersoni), Colorado tick fever and tularemia.

Question 254

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

Answer 254

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

Question 255

5 DON’Ts of rickettsial disease

Answer 255

• 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

Question 256

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

Answer 256

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.

Question 257

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!

Answer 257

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

Question 258

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

Answer 258

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 +

Question 259

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

Answer 259

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

Question 260

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

Answer 260

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

Question 261

•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)

Answer 261

Rickettsia prowazekii

Question 262

• 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

Answer 262

Rickettsia parkeri

Question 263

• 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!

Answer 263

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

Question 264

identify treatment of ricketssia and oriental infections

Answer 264

•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

Question 265

Treatment of pediatirc RMSF?

Answer 265

•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

Question 266

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

Answer 266

Ehrlichia and Anaplasma

• Morula: microcolony of Ehrlichiae within a vacuole
• Ehrlichia chaffeensis→ human monocytic ehrlichiosis (HME)
• Anaplasma phagocytophilum →human granulocytic anaplasmosis (HGA)

Question 267

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

Answer 267

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

Question 268

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

Answer 268

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

Question 269

identify lab finding in anaplasma and ehrlichia

• WBC count
• lymphocytes
• plateles
• liver

**treatment and prevention

Answer 269

• 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

Question 270

identify 3 types and what they cause

• Weakly staining, gram Neg spirochetes
• Motile (flagella)
• Very difficult to cultivate

Answer 270

Borrelia

• B. recurrentis→ Epidemic relapsing fever
• Borrelia spp→ Endemic relapsing fever

•B. burgdorferi→ Lyme disease

Question 271

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

Answer 271

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

Question 272

How do you diagnose lyme disease (borrelial burgdorferi)

**2 steps (specific vs not very specific)

• best way to diagnose?

Answer 272

• 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!

Question 273

Treatmenet of lyme disease

**Based on?

• associated conditions tp treat (CNS, carditis, recurrent arthritis)

Answer 273

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

Question 274

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

Answer 274

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

Question 275

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

Answer 275

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

Question 276

Identify condition

Not a bacteria but protoza

•Forms:

–Sporozoite (ticks), trophozoite→merozoite→gamete

•Intra-erythrocytic parasite

–Yes, like malaria!

Answer 276

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

Question 277

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

Answer 277

Babesia

•Risk factors for severe babesiosis include: asplenia, advanced age, and other causes of impaired immune function (e.g. , HIV, malignancy, corticosteroid therapy)

Question 278

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

Answer 278

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

Question 279

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

Answer 279

• 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)

Question 280

Fracture Principles

History; acute vs stress fracture

PE; presentation? check skin for? if high energy - evaluate for?

Answer 280

•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

Question 281

Fracture workup

1. best imaging to order
2. what is used for difficult 3-D fractures
3. which is most sensitive

Answer 281

–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.

Question 282

Identify 4 R’s in the treatment of fractures

Answer 282

–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

Question 283

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

Answer 283

–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!

Question 284

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?

Answer 284

•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

Question 285

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)

Answer 285

Nonunion

Question 286

3 types of bone grapft

Answer 286

–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

Question 287

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

Answer 287

–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.

Question 288

2 groups of Treatment option of fracture type

1. involves joint surface
2. Does not involve joint surface

Answer 288

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

Question 289

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

Answer 289

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

Question 290

identify pro (4) and con (2) of casting

**what type of bon ehealing occurs?

Answer 290

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

Question 291

Identify pro (2) and con (3) of traction

Answer 291

Traction

Pro

Doesn’t disturb fracture milleu

No risk of surgery

Con

Poor reduction

Pin site problems

Fracture Disease

Question 292

Pro (4) and con (3) of IM (intramedullary nailing)

Answer 292

IM Nailing

•Pro

–Load bearing

–Small incisions

–Periosteal blood supply ok

–Stimulates endosteal blood supply

•Con

–Not anatomic

–Callus formation

–Too much movement?

Question 293

Identify pro(4) and con (2) of ORIF

Answer 293

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

Question 294

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

Answer 294

ORIF Locked

Question 295

Pro (2) vs con (1) of weight bearing status - less movement (race against fatigue failure)

Answer 295

•Pro

–Quicker return to function

–Stimulates bone growth

•Con

–May be more weight than fixation can handle

Question 297

Pro (4) vs con (2) of movement (after fracture treatment)

Answer 297

•Pro

–Faster return to function

–Decrease stiffness

–Faster healing

–Helps reduction of fractures

•Con

–Wound problems

–May overwhelm fixation or repair

Question 298

1. describe compartment syndrome
2. define non-union
3. are IM nails load sharing

Answer 298

• 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

Question 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

Answer 299

• 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

Question 300

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

Answer 300

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

Question 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

Answer 301

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.

Question 302

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

Answer 302

Osgood Schlatter

—Treatment

¡NSAIDs, rest, PT

Question 303

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

Answer 303

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

Question 304

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

Answer 304

Perthes Disease —Idiopathic osteonecrosis of femoral head, between 4-8 yo.

—Treatment

¡ROM and bracing. No good treatment.

Question 305

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

Answer 305

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

Question 306

Identify condition

—Symptoms

¡Worried parents

—Exam

¡Measure knee angle

—Tests

¡Weight bearing Xrays if outside normal

—Treatment

¡Observation, bracing, occasional epiphyseal stapling, osteotomy

Answer 306

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)

Question 307

Identify condition and treatment

—Symptoms

¡Pain, limp, frequent ankle sprains

—Exam

¡Restricted hindfoot movement

—Tests

¡Xrays will show navicular coalition. CT scan can confirm

Answer 307

Tarsal Coalition; Abnormal connection between tarsal bones

Question 308

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

Answer 308

Transient synovitis of the hip; sterile effusion of hip causing pain

**Treatmnet - supportive care

**rule out septic arthritis

Question 309

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

Answer 309

Supracondylar Humerus Fracture

—Treatment

¡Casting vs surgical reduction

Question 310

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

Answer 310

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.

Question 311

what part of UE and LE gets most of the growth

Answer 311

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

Question 312

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)

Answer 312

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

Question 313

Identify classification of growth plate injuries (type I to IV)

Answer 313

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

Question 314

Identify condition

• Mono articular
• Oligoarticular
• Systemic symptoms
• JIA (painless single joint), Lyme, Septic
• Ophthalmology consult?
• Sometimes painless

Answer 314

Acute joint effusion (knocked knee)

Question 315

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.

Answer 315

Cerebral Palsy

Question 316

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

Answer 316

Achondroplasia

•FGFR-3 Mutation

Question 317

Identify condition

- fibrillin mutation****

**Long fingers and narrow bones

Answer 317

Marfan’s Syndrome

Question 318

identfiy condition and treatment

• Defect in collagen I from osteoblasts
• Sx

•Blue sclerae, macrocephaly, hearing loss, poor dentition, kyphoscoliosis, fracture, growth retardation

Answer 318

Osteogenesis Imperfecta

Treatment; •Bisphosphonates, surgery

Question 319

1. genetic mutation of achondroplasiia
2. vitamin deficiency of rickets
3. risk factors of SCFE (slippec carpital femoral epiphysis)

Answer 319

• 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

Question 320

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

Answer 320

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.

Question 321

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.

Answer 321

RHEUMATOID ARTHRITIS - refer to rheumatology – started Embel (etanercept)

RA (NSAIDS, DMARDS, Steroid).

Question 322

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)

Answer 322

Osteosarcoma – Neoadjuvant chemo (doxorubicin, cisplatin, MTX), wide resection, reconstruction and chemo.

Question 323

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

Answer 323

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)

Question 324

what causes disc herniation (3)

Answer 324

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

Question 325

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.

Answer 325

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)

Question 326

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)

Answer 326

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)

Question 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

Answer 327

Missed femoral fracture Grade IV. Treated with Hemiarthroplasty

Question 328

1. what artery supplies femoral neck
2. treatment of osteoporosis
3. tx of avascular necrosis
4. tx of osteomalacia

Answer 328

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)

Question 329

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

Answer 329

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.

Question 330

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).

Answer 330

OSTEOGENESIS IMPERFECTA TYPE I

Treatment and test; Bisphosphate (do skin biopsy to test collagen)

Question 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?)

Answer 331

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

Question 332

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?

Answer 332

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

Question 333

How does gout elicit an inflammatory response to become acute arthritis

**what 3 things occur if left untreated?

Answer 333

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.

Question 334

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?

Answer 334

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

Question 335

Identify 3 non-drug therapy of gout

• weight?
• water?
• alcohol

Answer 335

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

Question 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

Answer 336

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.

Question 337

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)

Answer 337

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.

Question 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

Answer 338

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.

Question 339

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**

Answer 339

Rasburicase (Elitek)

Toxicity-hemolysis in GGPD deficient patients, methemoglobinemia, acute renal failure and anaphylaxis have been observed.

Question 340

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.

Answer 340

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. To 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.

Question 341

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.

Answer 341

Benzbromarone (Exurate)

Question 342

Identify 2 extra drugs for gout

**Both anti-inflammatory agents

Answer 342

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.