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ABOS1 > General > Flashcards

General Flashcards

1
Q

What are some of the most predictive factors of death within orthopaedic surgery?

A

Chronic renal failure, CHF, COPD, hip fractures, and age greater than 70 yrs. Karaeminogullari et al found that hip fracture in patients on chronic hemodialysis had a 2 year mortality rate of 45%.

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2
Q

Causative pathogen of Lyme Disease?

A

spirochete Borrelia burgdorferi.

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3
Q

Treatment for acute lyme disease?

A

doxycycline.

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4
Q

What are the three stages of lime disease and how long do they last?

A

Stage 1: rash 1-30 days after bite.

Stage 2: Neurologic and cardiac. Weeks and months after bite. 15-20% of untreated patients. Lyme cartitis is rare.

Stage 3: Arthritis, usually the knee. Months to years. 60% of untreated patients.

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5
Q

What is different between Bell’s Palsy and CN VII palsy from Lyme disease?

A

Bilateral 50% in Lyme disease.

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6
Q

What study(s) is used to confirm Lyme disease?

A

ELISA positive and Western blot Positive.

Vaccination will not have a Western blot.

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7
Q

What is the mechanism of doxycycline?

A

Inhibits the 30s ribosomal subunit.

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8
Q

Inheritance pattern for Neurofibromatosis type 1?

Mutation?

A

Autosomal dominant.

NF1 gene.

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9
Q

What percentage of ulcers that probe to bone are associated with osteomyelitis?

Are bone biopsies indicated?

A

2/3.

Yes, despite us never doing them.

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10
Q

what is the inheritance pattern of achondroplasia?

What is the mutation?

A

autosomal dominant

FGFR3

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11
Q

What is sequestrum?

A

The necrotic bone that becomes walled off from its blood supply.

Becomes a nidus for chronic osteomyelitis.

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12
Q

What is involucrum?

A

A layer of new bone growth outside existing bone.

Seen in osteomyelitis.

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13
Q

What inflammatory marker is most sensitive to monitor therapeutic response to treatment of an infection?

A

CRP

elevated within 6 hours. ESR rises much more quickly.

Should decline after 48-72 hours of treatment.

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14
Q

Is procalcitonin low or high in the following situations?

Bacterial infection?

Viral infection?

Inflammatory conditions?

A

High

Low

Low

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15
Q

When is pharmacologic treatmetn of osteoporosis indicated?

A

DEXA T-score between -1.0 and -2.5 at the femoral neck/spine AND 10 year risk of hip fracture >= 3% OR 10 year risk factore of major osteoporosis-related fracture of >= 20% as calculated by FRAX

DEXA T-score -2.5 or less

Prior hip or vertebral fracture

PATIENTS MUST BE POST-MENOPAUSAL WOMEN OR MEN > 50 YRS

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16
Q

Describe the gait cycle.

A
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17
Q

What is the difference between CRPS 1 and CRPS 2?

A

CRPS Type I is symptoms in the entire extremity.

CRPS Type 2 is symptoms in a single nerve distribution.

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18
Q

True or Flase gender is not a risk factor for Elder abuse?

A

True

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19
Q

Bruises from elder abuse are?

A

commonly over 5cm in size.

located on the face, neck, or back.

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20
Q

What percen of women experience some form of domestic violence?

males?

Children in homes where domestic violence occurs?

A

25%

15%

50%

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21
Q

Does a physician have a duty to report domestic abuse?

A

ethically yes but reporting requirements are not standardized among states.

A physician does not have authority to provide protection to abused spouses in most states.

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22
Q

Where are two common locations for osteomyeltis in dialysis patients?

A

Spine and ribs.

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23
Q

Most common site of osteomyelitis that occurred by hematogenous spread in adults?

A

Vertebrae

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24
Q

What is the recurrence rate of despite surgical debridement and long-term antibiotics of osteomyelitis in adults?

A

30%

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25
Q

What organism is most likely in an IV dug abuser with AC or SC joint infections?

A

Still Staphylococcus aureus

Pseudomonas.

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26
Q

How much bone loss must there be in acute osteomyelitis before it is evident on plain films?

A

50%

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27
Q

What is a penumbra sign?

A

Dark central abscess with bright internal wall and dark external sclerotic rim on T1 sequence of an MRI.

Found in patients with osteomyelitis.

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28
Q

What is the gold standard culture for guiding abx therapy in osteomyelitis?

A

Bone culture.

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29
Q

What are the benefits of vacuum-assisted wound closure?

A

Remove insteritital fluids that contain inhibitory factors on healing.

Removal of the excess fluid pulls out excess proteins and electrolytes to help maintain an osmotic and oncotic gradient.

Decreases capillary afterload which promotes better blood inflow.

Micromechanical forces exerted on individual cells causes a release in local growth factors such as VEFG.

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30
Q

What is a common organism in patients with HIV other than staph aureus?

A

Baronella Henselae

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31
Q

What pathogen is suspected in cases of human bites?

A

Eikenella corrodens

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32
Q

What WBC count is consistent with a native spetic arthritis?

A

WBC > 50,000

Gram stains only identify infective organism 1/3 of time

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33
Q

What percent should the glucose level of a joint aspirate be of serum glucose level?

A

Less than 60%

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34
Q

How much saline for the knee is needed to determine an arthrotomy with 95% sensitivity?

99% sensitivity?

A

155ml

175ml

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35
Q

How long before Biofilm production usually occurs?

A

4 weeks.

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36
Q

What is the mortality rate of necrotizing fascitis?

A

32%

Correlates with time to surgical intervention

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37
Q

What is the most common adult brachial plexus injury?

A

Complete with involvement of all roots.

75-80% of traumatic brachial plexus injuries.

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38
Q

Do uppper or lower plexus injuries have an improved prognosis?

A

Upper, becuase they have preservation of hand function.

Recovery of reconstructed plexus can take up to 3 years.

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39
Q

What lesions suggest a preganglionic plexus injury?

A

Horner syndrome- due to disruption of sympathetic chain.

Winged scapula medially(inferior border goes medially)-loss of serratus anterior(long thoracic) and rhomboids(dorsal scapular nerve)

flail arm but sensory intact

Elevated hemidiaphragm(phrenic nerve)

Lattissimus dorsi, supraspinatus, or infraspinatus injury.

Normal histamine test (C8-T1 sympathetic ganglion)-intact triple response (redness, wheal, flare)

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40
Q

What is normal cervical paraspinal muscle activity on EMG characteristic of?

A

Post-ganglionic injury.

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41
Q

What does fractures of the first or second rib suggest?

A

Possible damage to overlying brachial plexus.

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42
Q

What is gold standard for defining a nerve root injury as oppossed to a plexus injury?

A

CT myelogram. Scan should be done 3-4 weeks after injury. This gives time for blood clot to resorb and characteristic meningocele to form.

MRI for plexus injuries.

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43
Q

What findings on MRI are consistent with brachial plexus injury?

A

pseudomeningocele. T2 will show increased water content in a pseudomeningocele.

Empty nerve root sleeves. T1 images demostrate the fat in the empy nerve root sleeves

Cord shift away from midline.

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44
Q

What is significant about fibrillation potentials on EMG?

A

show up when there is denervation.

In plexopathies as early as 10-14 days for proximal muscles and as late as 3-6 weeks in distal muscles.

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45
Q

What are the signigicance of SNAPs in a brachial plexus injury?

What test is needed along with the EMG?

A

SNAPs = sensory nerve action potentials

Obtained from nerve conduction velocity.

SNAPs are preserved in lesions proximal to dorsal root ganglia. So it helps distinguish preganglionic from postganglionic lesions.

For example if a patient is insensate in the ulnar nerve distribution but has a normal SNAP this is consistent with a preganglionic injury to C8 and T1.

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46
Q

What are nerve action potentials(NAP) used for.

A

Test the nerve accross a lesion.

Often intraoperative

Can detect reinnervation months before EMG

NAP postivie across a lesion signifies preserved axons or signficant regneration.

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47
Q

What physical exam finding is the best clinical sign of effective nerve regneration in a plexopathy?

A

Advancin Tinels sign.

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48
Q

What is neurotization?

A

Nerve transfer

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49
Q

When is immediate surgical exploration indicated for brachial pexus injury?

A

Sharp penetrating trauma. This doesn’t include gun shots.

Iatrogenic injuries.

Open injuries

Progressive neurologic deficits

Expanding hematoma or vascular injury.

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50
Q

When is delayed surgical intervention indicated for adult brachial plexus injuires(3-6 months)?

A

Partial upper plexus involvement and low energy mechanism.

Plateau in neurolgic recovery

Do not wait beyond 6 months.

At this point usually invovles tendon/muscle transfers to restore function.

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51
Q

What are the priorities of repair or reconstruction for muscle and tendon transfers in brachial plexus injuries?

A

Elbow Flexion

Shoulder stability

Brachial thoracic pinch

C6-C7 sensory (lateral cord)

Wrist extension/finger flexion (lateral and posterior cords)

Wrist flexion/finger extension

Intrinsic function

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52
Q

What should be done prior to any surgery on a patient with Marfan Syndrome

A

Cardiology consultation.

Echocardiogram.

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53
Q

What medication can decrease the risk of aortic dilation in a patient with Marfan Syndrome?

A

Beta Blockers.

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54
Q

Can intracranial pressure (ICP) be elevated because of pain?

A

Yes

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55
Q

Are peripheral nerve injuries more common in open or closed fractures?

A

More common in closed fractures.

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56
Q

How far from the knee joint can a gastrocnemius flap provide coverage?

A

15cm

Lateral gastroc is generally smaller and has less excursion.

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57
Q

What bacteria do you expect most from a human bite?

A

Eikenella

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58
Q

What are the cardiac effects of hypothermia?

A

Initially tachycardia then ->

Decreased BMR, HR. and Cardiac output

Myocardial irritability

Will have an abnormal EKG

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59
Q

What are the neurological effects of hypothermia?

A

Disorientation, coma

Anaerobic shivering until core temp drops below 30-32

Below this temp shivering stops and muscle rigidity ensues.

Resembles death they have absent respirations, dilated pupils, and rigor mortis

Must rewarmed before pronounced dead.

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60
Q

what is the classification for frostbite?

A
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61
Q

What treatment is recommended for frostbite?

What is an adjunctive treatment that can be used for severe frostbite with no blood flow on bone scan but has severile contraindications?

A

Resuscitation with warm I fluids, tetanus prophylaxis, NSAIDs, silver sulfadiazine ointment, topical antibiotics to open wounds, and rapid rewarming with 40-42C water bath with mild antibacterial agent for 30 minutes. Do this until skin becomes pliable and red-purple.

Debride clear blisters.

Drain/aspirate hemorrhagic blisters.

Late debridement/amputation after demarcation occurs at 1-3 months.

intravenous tPA within 24 hours can reduce rates of digital amputations.

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62
Q

What complications are seen from frostbite in adults?

What else can be seen in pediatric patients?

A

Persistent pain 50%

Cold intolerance

Vasospastic disease that can present late. Can be treated with calcium channel blockers, vasodilators, beta blockers, and surgical sympathectomy.

Joint contractures

Premature growth plate closure that can occur 1-2 years after exposure. Can lead to joint laxity, angular deformities, short digits, excess skin, and degenerative joint changes.

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63
Q

What is classified as a thin, intermediate, and thick ski graft?

A

Thin- .005-.012 inch

Intermediate- .012-.018

Thick- .018-.030

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64
Q

Should subcutaneous fat be included for full-thickness skin grafts?

A

No, because it decreases vascular ingrowth and survival.

Takes 2 to 3 days to revascularize.

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65
Q

Describe the regeneration process after nerve transection?

A

Distal segment undergoes Wallerian degeneration (axoplasm and myelin are degraded distally by phagocytes)

Existing Schwann cells proliferate and line up on basement membrane.

Proximal budding occurs after 1 month delay.

Leads to sprouting axons that migrate at 1mm/day to connect to the distal tube

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66
Q

What factors affect the success of recovery following repair of a peripheral nerve?

A

#1 Age- Single most important factor

Level of injury- the more distal the better

Sharp transection vs crush

Repair delay- time limit for repair is 18 months.

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67
Q

Free tissue transfer after a severe upper extremity trauma in the upper extremity should occur after how many hours to minimize complications?

A

72 hours

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68
Q

What is an axial pattern local flap?

A

Single arteriovenous pedicle (a named vessel)

length-width ratio needed > 2:1

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69
Q

What is a random pattern flap?

A

Supported by numerous microcirculation with no single arteriovenous pedicle.

Length-width ratio needed < 2:1

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70
Q

What is a venous flap with regards to soft tissue coverage of defects?

A

uses veins as inflow and outlfow of arterial blood.

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71
Q

Describe following leg muscle flaps in the image reagarding their use, blood supply, and any structures at risk?

A
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72
Q

Describe the following bone flaps in the image regarding their use and blood supply.

A
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73
Q

When do most VTE events after major hip or knee surgery occur?

A

2-6 weeks after surgery.

After hosptial discharge.

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74
Q

What is the optimal timing for stage 2 of the Masquelet technique?

A

4-6 weeks following stage 1

Highest amount of BMPs, VEGF, and IL-6 expressed from the membrane at that time.

Big advantage of the membrane is that it prevents resorption of the bone graft

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75
Q

What is a complication after a person recovers from heat stroke?

How long can it last?

A

Heat sensitivity

1 year

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76
Q

What is the definition of heat stroke?

A

hyperthermia with body temperature above 40.5 degrees celsius

Anhidrosis

Central nervous system dysfunction

Tachypnea

Tachycardia

Heat exhaustion is a core temperature less than 39 celsius with absence of central nervous system dysfunction.

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77
Q

Define the various types of muscle movements and give an example.

A
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78
Q

For Anaerobic, Glycolytic, and Aerobic define the following:

Energy source

Muscle type

Exercise Duration

A
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79
Q

What muscle fibers increase over time with endurance training?

A

Increase in the percentage of more highly oxygenated Type IIA fibers.

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80
Q

With regards to exercise science what is periodization?

A

Planned variation in intensity and duration of a specific workout over a predefined duration of time.

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81
Q

What is exercise induced laryngeal obstruction (EILO)?

A

obstruction due to supraglotic(arytenoids and supporting structures) or glottic (vocal cords) level of the larynx.

Diagnosed by a negative bronchodilator reversibility test (with beta2-agonist) and a negative bronchoprovocation test. Both of which would be positive in exercise induced bronchoconstriction.

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82
Q

Muscle strains most commonly occur at what area of the muscle?

What type of contraction does it most commonly occur with?

A

Myotendinous junction.

Eccentric contraction.

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83
Q

What is the recommended treatment for a partial muscle laceration?

A

3-5 days of immobilization followed by an exercise and ROM program.

More prolonged immobilization will lead to fatty atrophy and disordered healing.

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84
Q

True or False atrophy is more prominent if immoblization occurs without tension?

A

Ture.

Quadriceps atrophy greater than hamstrings with knee immobilization in extension.

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85
Q

What is hyphema?

Treatment?

A

Blood in anterior chamber

May represent vitreous or retinal injury

Place eye patch and refer to ER or Optho.

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86
Q

What are symptoms of retinal detachment?

A

Bright flashes, stabbing pain, and visual field cut.

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87
Q

Diagnosis and treatment for a corneal abrasion?

A

Diagnoses with fluorescent stain and UV light.

Treat with topicla antibiotics, topical NSAIDs, eye patch, and nonurgent referral to opthalmologist.

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88
Q

What is traumatic mydriasis?

Treatment?

A

A transient phenomenon during which the iris fails to contrict properly, resulting in a dilated pupil.

Caused by a contusion to iris sphincter.

Treated with bedrest.

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89
Q

What is commotio cordis?

A

Disrupted cardiac conduction as a result of a blow to the chest.

More common in young children such as a little league batter hit in the chest with a pitch.

Fatal unless immediate cardiac defibrillation is performed.

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90
Q

What murmur warrants further work-up on pre-participation physical?

A

Any diastolic murmur warrants further work-up

Grade II or greater systolic murmur.

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91
Q

Which of the following are normal EKG findings in endurance athletes?

A

Ventricular hypertrophy

Primary AV block

Nonspecific STT- wave changes in the lateral leads on EKG.

Resting sinus bradycardia at 40 beats per minute

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92
Q

True of false hypertrophic cardiomyopathy is an absolute contraindication to vigorous exercise and sports?

A

True

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93
Q

What murmur is concerning for hypertrophic cardiomyopathy?

A

A murmur that increaes with standing or valsalva maneuver

Will be a systolic murmur

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94
Q

What is long QT syndrome?

Symptoms

A

An abnormality of ventricular repolarization that can lead to ventricular tachycardia, torsades de pointes, and sudden cardiac death if not recognized and treated

Symptoms are syncope or near-syncope with exercise.

Diagnosed by ECG.

Return to play on a case by case basis.

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95
Q

Which viscera are more likely to undergo deceleration injuries?

A

Spleen, liver, and kidnery.

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96
Q

What may cause acute abdominal pain with nausea, vomiting, and pain with active trunk flexion or rotation?

A

Rectus sheath hematoma.

Symptoms mimic surgical abdomen.

Diagnosis can be made with a CT which can rule out other injuries as well.

Caused by injury to epigastric or intramuscular vessels.

Treat with ice and rest unless symptoms are perisstent.

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97
Q

Will a hematocoele transilluminate?

A

Hematocoele is a rupture of tunica albuginea (outer covering)

Causes a painful firm scrotal mass

does not transilluminate

Diagnosis with ultrasound.

Treatment observation.

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98
Q

What is initial treatment for small MRSA lesions in athletes?

A

Mupirocin

Larger lesion Bactrim and rifampin with I&D.

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99
Q

What is the most likley dianosis for a wrestler with a cluster of fluid-filled blisters?

A

Herpes

2-7% of wrestlers.

100
Q

Return to play for athletes with herpes?

A

Need to be treated with acyclovir or valacyclovir.

No new lesions within the preceding 72 hours.

At least 5 days of anit-viral medications.

Lesions should be scabbed over.

101
Q

What is tinea cruris?

A

Fungal infection that affects genitals, inner tighs, and buttocks. Jock itch

102
Q

What study can be used to diagnose tinea corporis?

A

Scrapings from lesions are examined under microscope after preparation with potassium hydroxide.

Positive for tinea if hyphae are found.

103
Q

Return to play for athletes with tinea infections?

A

After 48 hours of treatment.

104
Q

Common pathogens of impetigo?

Treatment?

Return to play?

A

Streptococcus pyogenes and staphylococcus aureus.

Topical bactroban and erythromycin.

May return to play when all lesions are clear of crusting.

105
Q

What is the incubation period for mononucleosis?

A

30-50 days

106
Q

What is Hoagland’s triad?

A

Found in patients with mononucleosis.

Fever.

Pharyngitis- Exudative (white/grey pseudomembrane) in 50%. Group A streptococcus is responsible.

Lymphadenopathy- Posterior cervical chain lasts 2-3 weeks.

107
Q

How long do symptoms of mononucleosis usually persist?

A

4-8 weeks.

108
Q

What symptoms are present in the prodromal period of mononucleosis?

How long does it last?

A

Malaise, myalgia, nausea, and headache.

3-5 day prodromal period

109
Q

Studies to diagnose mononucleosis?

A

Heterophile Ab test (Mono-spot test)

Viral capsi antigen (VCA) IgG and IgM. More sensitive and specific.

Absolute and relative lymphocytosis with > 10% atypical lymphocytes.

110
Q

Treatment for mononucleosis?

A

Hydration, acetaminophen, and rest.

IM (one time) or PO (10 days) penicillin for strep pharyngitis. Do not use amoxicillin but erythromycin if allergic to PCN.

Corticosteroids to decrease tonsillar size if there is difficulty swallowing and dehydration.

Stool softener to decrease valsalva maneurver which exacerbate splenomegaly

111
Q

How long before an athlete can return to play if they have mononucleosis?

A

3-5 weeks. Can take up to 3 months.

Athletes with splenomegaly cannot return to play until it has resolved.

Most splenic ruptures occurs in first 3 weeks.

112
Q

How do splenic ruptures occur in athletes with mononucleosis?

A

Due to sudden increase in portal venous pressure.

50% from external trauma (football tackle)

50% atraumatic from Valsalva maneuver (rowing or lifting)

113
Q

An athlete with HIV should be prohibited from competition?

A

False, insufficient grounds.

114
Q

What is requried for a diagnosis of AIDS?

A

HIV positive test and one of the following:

CD4 count less than 200.

Diagnosis of an opportunistic infection.

115
Q

Complications from mononucleosis?

A

Splenic rupture

Aplastic anemia

Guillain-Barre syndrome

Meningitis/encephalitis

Neuritis

Lymphoma

Hemolytic uremic syndrome

Disseminated intravascular coagulation.

116
Q

Diagnosis for asthma?

A

Low forced expiratory volume in 1 second (FEV1) and low FEV1/FVC ratio.

Improves with administration of bronchodilators.

+/- bronchial provocation challege with methacholine.

117
Q

What is the difference between exercise induced bronchospasm and exercise-induced asthma?

A

EIA occurs in patients with an underlying diagnosis of asthma where exercise is the tigger.

EIB occurs in athletes with no underlying asthmatic disease.

118
Q

What is pseudo-asthma syndrome?

A

Hyperventilation during exercise that causes respiratory symptoms (wheezing, chest tightness).

Not related to bronchial constriction.

119
Q

Diagnosis for exercise induced bronchospasm (EIB)?

A

Eucapnic voluntary hyperventilation test: Gold standard. Patient hyperventilates dry gas with a % carbon dioxide level to mimic exercise conditions. Spirometry findings > 10% reduction in FEV1 is diagnostic.

Improves with administration of bronchodilators.

PFTs can be normal at baseline.

120
Q

Treatment for Exercise-Induced Laryngeal Obstruction (EILO)?

A

Laryngeal control therapy.

Speech therapy.

SSRIs.

Botulinum toxin injections.

121
Q

What is exercise-induced anaphylaxis?

A

Rare light-threatening systemic hypersensitivity response triggered by physical exertion.

Type I hypersensitivity reaction (IgE mediated).

Can be preceeded by ingestion of food allergen prior to exercise.

In addition to breathing difficulties patients will have pruritis and urticaria. Also can have abdominal pain, nausea, vomiting, and cramps.

122
Q

What will you find on physical exam of someone with a tension pneumothorax?

A

Visible deviation of trachea and jugular venous distension

Tachypnea and tachycardia

Unilateral decreased or absent breath sounds

Hyperresonant to percussion

123
Q

What will you see on ultrasound of a patient with a pneumothorax?

A
124
Q

For an adult patient with a tension pneumothroax what is initial treatment?

For a pediatric patient?

A

Placement of a needle into the fifth intercostal space in the midaxillary line.

Second intercostal space, midclavicular line for pediatric patients.

Then transport to and ER for placement of a chest tube.

125
Q

Treatment for a pnuemothorax that isn’t a tension pneumothorax?

A

If pneumothorax > 20% (lung edge > 2cm from chest wall) -> Chest tube placement and admission to hospital.

If pneumothorax < 20% and patient clinically stable -> observe for 4-6 hours. Supplemental oxygen increases rate of pleural air absorption and can accelerate resolution. Repeat CXR prior to discharge from observation and at 12-48 hours post-discharge.

No flying for 2-4 weeks. Decreased pressure on airplane can increase volume of pneumo.

Return to play is 4 weeks folliwng resolution of pneumothorax.

126
Q

When should a hemothorax with a chest tube placed undergo VATS or thoracostomy?

A

>1500cc initial chest tube output

>200cc/hr for 3+ hours

Increasing size of hemothorax.

Incomplete resolution despite 2 chest tubes.

127
Q

Why are athletes thought to be at increased risk of PE?

A

Higher rate of injuries leading to immobilization.

Athlete specific repetitive motions such as ptiching and serving.

Frequent long distance travel.

128
Q

Treatment for an athlete with a PE?

Return to play?

A

Systemic anticoagulation for 3-6 months. Intravenous or lovenox that is subsequently converted to an oral anticoagulant.

Average time 6 months.

Should not return to play while anticoagulated.

129
Q

Why are femlaes at a greater risk for ACL injuries?

A

Landing biomechanics (land in more extension and valgus due to hip internal rotation)

Neuromuscular control

Smaller notches and ACL sized

Cyclic hormonal levels- greater risk during the first half (preovulatory phase).

Leg alignment

Genetic predispostion- Underrepresentation of CC genotype of a COL5A1 gene sequence.

130
Q

What is the most common cause of amenorrhea in femal eathletes?

A

Insufficient caloric intake

Secondary amenorrhea is degined as cessation of menses for 6 months after at least one normal cycle.

131
Q

Treatment for the femlae athlete traid (Anorexia athletica)?

A

Multidisciplinary approach that should include:

Psychological couseling.

Dietary management.

Reduced training intensity.

Oral contraceptive pills.

132
Q

side effects of anabolic steroids?

A

Hypertension

Liver tumors

Increased LDL

Decreased HDL

Hypercholestrerolemia

Aggressive behavior

Oligospermia or azoospermia

Decreased bone mineral density

133
Q

A blood test consistent with anabolic steroid use would show?

A

Testosterone to epitestosterone ratio of > 6:1

134
Q

List the various types of steroids?

A

HGH- Anabolic steroid substitute. Accelerates the incorporation of amino acids into proteins. Increased muscle size but not strength. Side effects: myopathic muscles (do not function properly) development, carpal tunnel syndrome, and insulin resistance.

Androstenedione- Androgen produced by the adrenal glands and gonads. Converted by the liver directly to testosterone.

DHEA- Made by adrenal cortex. It is converted into androstenedione.

Somatotropin- A growth hormone that causes hypertrophy of type 1 muscles and atrophy of type 2 muscles.

135
Q

What hormone is catabolic to muscles?

A

Glucagon.

136
Q

What is the mechanism of creatine?

A

creatine is converted to phosphocreatine which acts as a source of ATP for msucle.

Studies have shown that while it can increase work it cannot increase peak force.

Main side effect is cramps as it pulls water from blood vessels into cells.

137
Q

When is peak elution for antibiotic impregnated cement?

How long does the cement remain bactericidal?

A

1 day after placement

Up to 4 months.

elution duration is influenced by cement type.

138
Q

What is a ginglymus joint?

A

A hinge like joint that allows movement in only one plane.

Elbow

Ankle

139
Q

Common tendon transfers in RA?

A
140
Q

How is Rheumatoid elbow managed?

A

Mainly managed with medical management and cortisone injections.

Synovectomy and radial head excision- Often done if PIN compression secondary to radial head synovitis.

Interposition arthroplasty- youn patinets who are not candidates for TEA

TEA- semiconstrained device has best results. 5lb single arm weight lifting restriction lifetime.

141
Q

What are the two wrist conditions seen in patients with advanced Rheumatoid?

A

Caput-ulna syndrome- synovitis in the DRUJ > ECU subsheath stretching > ECU subluxation > supination of the carpal bones away from the head of the ulna > volar carpal subluxation > increased pressuve over the extensor compartments > tendon rupturs

Radiocarpal Destruction- synovitis and capsular distension leads to supination, radial deviation (angulation of carpus)

Ulnar and volar translocation of the carpus on the radius

With scaphoid flexion radiolunate widening, lunate translocation (ulnarwards)

Secondary radioscaphoid arthrosis

Ulnar deviation of the fingers at the MP joints creating the classic zigzag deformity

142
Q

What is the most prevalent inflammatory process affecting the shoulder?

A

Rheumatoid arthritis

90% of patients with RA will devleop shoulder symptoms.

Commonly associated with rotator cuff tears.

Classic radiograph findings:

Central glenoid wear

Periarticular osteopenia

cysts

143
Q

What is the most common manifestation of RA in the foot?

A

Toe hyperextenion deformity

Treatment is arthrodesis of the 1st MTP joint and lesser MTP joint resections

144
Q

What is podagra?

A

gouty arthritis of the great toe

145
Q

What is secondary gout?

A

Gout associated with a disease with high metabolic turnover (psoriasis, hemolytic anemia, leukemia, and chemotherapy).

146
Q

What is the pathophysiology of gout?

A

Dystunctional nucleic acid metabolism causing hyperuricemia and deposition of monosodium urate cystals in joints (a purine breakdown product).

Cyrstals lead to an inflammatory response activating proteases, protaglandins, leukotriene B4, and free oxygen radicals.

147
Q

What serum uric acid level is diagnostic of gout?

A

serum uric acid is not diagnostic of gout.

80% of people with an elevated uric acid will never have a gout attack.

148
Q

How is the diagnosis of gout made?

A

joint aspiration with crystal analysis

monosodium urate crystals- thin, tapered, needle-shaped intracellular crystals.

strongly negatively birefringent- Will be yellow(when aligned parallel to red compensator) and blue (when algined across the direction of polarization).

149
Q

What is the treatment for gout?

A

ACUTE: indomethacin 50mg TID. Colchicine in acute attacks if patient has a history of peptic ulcers.

If pateint unable to take NSAIDs or colchicine can give oral, intraarticular, or IV glucocorticoid steroids.

CHRONIC: Allopurinol (xanthine oxidase inhibitor) with colchicine for prophylaxis after recurrent attacks. 85% effective.

150
Q

What crystals are involved in pseudogout?

A

calcium pyrophophate dihydrate (CPPD) crystals

Mimics gout except:

Affects older patients > 60 years old

More proximal joints

Positively birefringent crystals. Rhomboid shaped.

151
Q

What may you see on radiographs of a patient with pseudogout?

A

Calcification of fibrocartilage stuctures. Chondrocalcinosis

TFCC in wrist

Meniscus in the knee

152
Q

What is the treatment for chronic pseudogout?

A

intraarticular yttrium-90 injections

Colchicine .6mg PO bid for recurrent cases for prophylaxis

Long term pseudogout can lead to permanent joint damage and renal disease.

153
Q

What is the neurovascular pathophysiology of a charcot joint?

A

Neuropathic patients have dysregulated reflexes and desensitized joints that receive signficantly greater blood flow.

The resulting hyperemia leads to increased osteoclastic resorption of bone.

154
Q

What is the most common cause of neuropathic arthropathy of the upper extremity?

Second most common cause?

A

Syringomyelia- 25% of charcot joints are a result of syringomyelia. Shoulder > elbow

Hansen’s disease (leprosy)

Other associated conditions with neuropathic arthropathy:

SHOULDER- Arnold-Chiari malformation, cervical spondylosis, adhesive arachnoiditis and TB arachnoiditis, post-traumatic syringomyelia, and alcoholism

ELBOW- Syringomyelia, syphilis, congenital insensitivity to pain, diabetes, and CMT.

155
Q

What imaging should be obtained when a patient presents with a neuropathic shoulder?

A

MRI of the cervical spine to rule out syrinx.

156
Q

What imagin study will be cold with a charcot joint but hot for osteomyelitis?

A

Indium leukocyte scan will be cold in charcot joint.

Hot for osteomyelitis.

Technetium bone scan is hot in both conditions.

157
Q

What is the operative treatment recommended for a neuropathic shoulder?

A

Arthrodesis but only perfomr during the quiescent stage. Cannot perform during the acute inflammatory stage.

Requires a very long period of immobilization.

Charcot joint is a contraindication to total joint replacement.

158
Q

What are the 5 patterns of psoriatic arthritis?

A

Asymmetric oligo/monoarticular arthritis affecting DIPJ, PIPJ, and MCPJ

DIP-predominant arthritis

Arthritis mutilans

Symmetric RF-negative polyarhtrits

psoriatic spondyloarthropathy

Affects up to 5-20% of patients with psoriasis

Affects men and women equally

HLAB27 found in 50%

159
Q

What is the physical signs of a patient with psoriatic arthritis?

A

Rash with silvery plaques over extensor surfaces. Typically preceds joint involvement by several years (80-85% of the time)

HANDS:

Dactylitis (sausage digit)

Onychodystrophy (nail pitting)

Onycholysis (lifting of nail plate starting distally)

Arthritis mutilans- also known as opera glass hands. See attached image

Chronic uveitis and entheses such as achilles tendonitis, posterior tibial tendonitis, and plantar fasciitis.

160
Q

What is the mainstay of treatment for psoriatic arthrits?

A

similar to RA

NSAIDs, methotrexate, sulfasalazine, cyclosporine, and TNF-alpha inhibitors.

Digit fusion vs resection arthroplasty for advanced joint disease.

161
Q

Who and what joint is mostly affected by hemophilic arthropathy?

A

young males between 3-15 years old.

Knee is most commonly affected. Elbow, ankle, shoulder, and spine are also involved.

Has decreased significantly due to home factor treatment.

162
Q

What should be screened for preoperatively before any surgical inteventions in a hemophiliac?

A

Presence of factor VIII inhibitors (including IgG antibodies)

IgG antibody inhibits response of therpaeutic factor treatment (monocolonal recombinant factor VIII)

Found in 5-25% of hemophiliac patients

Relative contraindication for surgical interventions.

163
Q

What are the three root bleeding disorders that are most commonly involved in hemophilic arthropathy?

A
164
Q

What will you see on radiographs of the knee in a patient with hemophilic arthropathy?

A

Squaring of the patella and femoral condyles (Jordan’s sign)

Ballooning of distal femur

Widening of intercondylar notch

Joint space narrowing

Patella appear long and thin on lateral

165
Q

What non-operative treatment is recommended for hemophilic arthropathy?

A

Compressive dressings, analgesics, short term immobilization followed by rehabilitation to prevent contractures. Steroids to help reduce inflammation.

FACTOR ADMINISTRATION:

PT- increase factor VIII to 20%

Acute hematomas- increase factor VIII to 30%

Acute hemarthrosis- increase factor VIII to 40-50%

Skeletal surgery- increase factor VIII to 100% for first week following surgery and maintain > 50% for second week following surgery.

166
Q

What is the operative treatment recommended for hemophilic arthropathy?

A

synovectomy- when recalcitrant to medical management. Limits pain and swelling and decreases recurrent hemarthroses.

synoviorthesis- failed medical management. Destruction of synovial tissue with intra-articular injection of radioactive agent. colloidal phophorus-32 chromic phosphate.

Total joint arthroplasty and arthrodesis are options in ends stage arthritis.

167
Q

What are the diagnostic criteria for fat emboli syndrome?

A

1 MAJOR: hypoxemia (PaO2 < 60)

CNS depression (changes in mental status

Petechial rash

Pulmonary edema

4 MINOR: tachycardia, pyrexia, retinal emboli, fat in urine or sputum, thrombocytopenia, decreased HCT.

168
Q

What are the symptoms and physical exam findings of fat emboli syndrome?

A

Symptoms usually present within 24 hours of inciting event.

Patients complain of feeling short of breath and appear confused.

Physical exam: tachycardia, tachypnea, petechia in axillary, conjunctivae, and oral mucosa.

169
Q

What is the treatment of fat emboli syndrome?

A

ACUTE: mechanical ventilation with high levels of PEEP

PREVENTION: early long bone fracture stabilization within 24 hours

TECHNIQUES TO REDUCE THE RISK OF FAT EMBOLI:

Overrreaming of the femoral canal during a TKA

Use of reamers with decreased shaft width reduces the risk during femoral reaming for intramedullary fixation.

Use of external fixation for definitive fixation of long vbone fractures in medically unstable patients decreases the risk.

170
Q

What is the epidemiology of Multiple Sclerosis?

A

20-40 years old

Women > Men

Norther latitude.

Not considered a hereditary disease

Environment found to more likely include stress, smoling, and decreased sunlight/ low vitamin D exposure.

171
Q

What are associated orthopaedic conditions of Multiple Sclerosis?

A

Increased fracture risk- due to increased risk of fails and osteoperosis

Osteoporosis- due to decreased physical activity, vitamin D deficiency, and immunomodulatory medication.

Gait abnormalities

Muscle and joint spacticity

172
Q

What is the most common pattern of disease progression in MS?

A

remitting-relapsing

173
Q

How is multiple sclerosis diagnosed?

A

Should be suspected based on physical exam.

CSF analysis: mononuclear pleocytosis (25%), Elevated CSF IgG (80%), and oligoclonal bands on electrophoresis.

Obtain MRI with gadolinium of brain and spinal cord. Findings of multiple areas of focal demyelination scattered in brian and spinal cord.

Also on imaging asymmetric periventricular plaques.

174
Q

What are the symptoms and history consistent with Multiple Sclerosis?

A

History: Clinically defined by two or more episodes of neurological dysfunction (brain, spinal cord, or optic nerves) that are separated in time and space.

Symptoms: PSYCH- fatigue depression, and mood disorders

CNS- optic neuritis, diplopia, nystagmus

ENT- dysarthria, dysphagia

MSK- weaness, loss of blabnce and coordination, spasms, ataxia, falls

NEURO- parasthesias, hypoesthesia, peculiar sensory phenomena’s (e.g. sensation of wetness)

GI- incontinenece, diarrhea, and constipation

UROLOGY- incontinence, frequency, and retention

175
Q

What on physical exam is consistent with multiple sclerosis?

A

Gain abnormalities (wide based, limb ataxia, or slapping foot)

Joint or muscle contractures

NEUROLOGIC: muscle spacticity, increased deep tendon relfexed, muscle weakness, Babinski positive

SPECIAL TESTS: Fundoscopy- MLF syndrome (internuclear ophthalmoplegia)

Lhermitte’s sign

176
Q

What is the treatment for multiple sclerosis?

A

Immunomodulators- coritcosteroids for acute exacerbations and prophylactic immunosuppresants (interferon beta)

Antispasticity agents

Physiotherapy

Osteoporosis management

177
Q

What is a progressive motor neuron disroder that involves the anterior horn cells of the spinal cord?

A

Amyotrophic Lateral Sclerosis (ALS)

Also referred to as Lou Gehrig’s disease.

While there is abnormal motor conduction there is normal sensory conduction.

178
Q

What are the symptoms and physical exam findings of ALS

A
179
Q

How to you diagnose ALS?

A

No laboratory test

EMG/NCS shows denervation + reinnervation. Normal sensory studies

Clinically is dependent on demonstration of both UMN and LMN involvement.

combination of UMN and LMN in the same extremity in the absence of pain and sensory symptoms.

Often misdiagnosed as cervical myelopathy or radiculopathy

180
Q

What is the treatment for ALS?

A

No cure or effective treatment.

Goal is to rpovide supportive care

Riluzole has been used but provides only a modest benefit. Prolongs life by 2-3 months.

Blocks tetrodotoxin-sensitive sodium channels associated with damaged neurons.

181
Q

What is the international asoociation for the study of pains classification of CRPS?

A

TYPE I: CRPS without demonstrable nerve damage. Most common. Results from trauma, casting, or tight dressings

TYPE II: CRPS with evidence of identigiable nerve dagmae. Minimal positive response with sympathetic blocks.

Another classfication system is the Lankfor and Evans Stages of RSD

182
Q

Prevention for CRPS?

A

Vitamin C 500mg for 50 days iwth distal radius fractures. Also been shown to work in foot and ankle surgery. 200mg dose if impaired renal function.

Avoid tight dressings and prolonged immobilization

183
Q

What are risk factors for CRPS?

A

Trauma with exaggerrated response to injury. Most common reason for poor outcome following a crush injury to the foot.

Surgery

Prolonged immobilization

Anxiety or depression

Use of ACE inhibitors at the time of trauma

History of migraines or asthma

SMoking

Fibromyalgia.

184
Q

True or False CRPS is thought to have a genetic component?

A

True

Associated with polymorphisms in TNF-alpha and ACE genes.

185
Q

What will a three-phase bone scan show in a patient with CRPS

A

Increaed uptake in all phases.

Phases III is most sensitive.

186
Q

What are the cardinal signs of CRPS?

What are the physical exam findings?

A

Exaggerated pain

Swelling

Stiffness

Skin discoloration

PHYSICAL EXAM: vasomotor disturbance, trophic skin changes, hyperhidrosis, flamingo gait if the knee is involved. Equinovarus deformity if the ankle is involved.

187
Q

How is CRPS diagnosed?

A

Usually clincial diagnosis but can be confirmed by pain relief with sympathetic block.

188
Q

Treatment for CRPS

A

See image

First line of treatment is physotherapy and phamacologic treatment.

Best success for surgical treatment with CRPS is if you can find an associated nerve problem and treat it.

189
Q

What medications are used to treat CRPS?

A

NSAIDs

Alpha blockers (phenoxybenzamine, prazosin)

Beta blockers

Anti-depressants

Anti-convulsants

Calcium channel blockers

Gabapentin

Bisphosphonates, anti-arrhythmics, corticosteroids, and calcitonin.

190
Q

True or false nitrous oxide use for general anesthesia leads to increased difficulty with fluoroscopic identification during pelvic and spinal procedures?

A

True

191
Q

What is the difference between in mechanism deploarizing and non-depolarizing neuromuscular blocking agents?

A

DEPOLARIZING: bind to, depolarize, and transiently block ACh receptor.

Short acting. No intermeidate or long acting.

Ex. Succinycholine

NON-DEPOLARIZING AGENTS: Bind to and transiently block ACh receptor, but do not depolarize

No short acting agents.

Intermediate-acting: rocuronium, vecuronium, atracurium, and cisatracurium

Long-acting: pancuronium

192
Q

Where would the following nerve blocks be anatomically given:

Lumbar plexus/Psoas compartment block?

Femoral nerve block?

Sciatic nerve block?

Obturator nerve block?

Popliteal nerve block?

Saphenous nerve block?

A

Lumbar Plexus forms the obturator nerve, LFCN, and femoral nerve. 3-5cm lateral to the spinous process of L4. Often guided by ultrasound and nerve stimulators.

Just lateral to the femoral artery on a line connecting the ASIS to the pubic symphysis.

Lines are drawn between the GT and PSIS. Then the GT and the sacral hiatus. Halfwary between the greater trochanter and the PSIS a perpendicular line is drawn, and the injection is palced where the perpendicular line corsses the line between the GT and the sacral hiatus.

Injection site is usually 2 cm inferior and 2 cm lateral to the pubic tubercle

site is often 10 cm proximal to the popliteal crease

Multiple techniques, but it is often blocked behind the sartorius msucle.

193
Q

What is hypotensive epidural anesthesia (HEA)

A

Epidural dermatomal block from T2 distal

Blocks cardio-accelerator fibers of sympathetic chain:

Causes bradycardia which is treated with low-dose epinephrine

Lowers MAP to 50mmHg

Keeps normal heart rae, CVP, stroke voluem, cardiac output

can be used in high risk patients with hypertension, poor cardiac function, and chronic kidney disease.

194
Q

Describe the inheritance, triggers, symptoms, outcome, and treatment of malignant hyperthermia?

A

autosomal dominant- abnormailities in the ryanodine receptor (RYR1) gene

TRIGGERS- volatile inhalational anesthetic agents and succinylcholine

SYMPTOMS- increased skeletal muscle contraction and metabolism (rigidity and masseter spasm). Rapid oxygen depletion. Increased carbon dioxide concentration (EtCO@) and body temperature.

Give dantrolene (calcium channel blocker) and provide active cooling.

195
Q

What is Local Anesthetic Systemic Toxicity (LAST)?

A

Comes from intravascular anesthetics.

CNS effects- seizures, coma, respiratory arrest

CVS effects- asystole, ventricular fibrillation, and cardiac arrest

antidote is intravenous 20% lipid emulsion

196
Q

Describe Bone cement implantation syndrome?

A

Hypotension and hypoxemia that occurs most often during arthroplasty with the use of bone cement.

Treatment is intravenous fluids, vasopressors, and 100% inspired oxygen.

197
Q

What is used to initiate platelet activation in the prepared sample of PRP?

A

Calcium chloride

Optimal concentration of PRP is 3-5x that of whole blood

>5x inhibits healing

198
Q

What are thr proposed beneftis of PRP?

What are the only two areas with literature that even supports some potential benefits.

A

Increase ECM deposition, reduce pro-apoptotic signals, and minimzie joint inflammation.

Due to release of growth factors: PDGF, TGF-B, VEGF, IGF-1, EGF, CTGF, and FGF-2.

BPTB donor sites in ACL reconstruction and tennis elbow.

199
Q

What is the EuroQol-5D (EQ-5D)?

A

outcome measure tool that assesses generic health status/quality of life

available in 170+ languages.

200
Q

Describe the Hospital Consumer ASsessment of Healthcare Providers and Systems (HCAHPS)

A
201
Q

Desribe the Disabilities of the Arm, Shoulder, and Hand (DASH) Score

A
202
Q

What factors increase radiation exposure levels during use of fluoroscopy?

A

Imaging large body parts.

Positioning extremity closer to the x-ray source.

Use of large c-arm instead of the mini c-arm.

203
Q

What factors decrease radiation exposure to patient and surgeon?

A

Maximizing the distance between the surgeon and the radiation beam.

Minimizing exposure time.

Manipulating the x-ray beam with collimation.

Orienting the fluoroscopic beam in an inverted position relative to the patient.

Strategic positioning of the surgeon within the operative field to avoid direct path of beam.

Use of protective shielding during imaging.

204
Q

What is the risk os seroconversion for the following?

HIV needlestick?

HIV exposure to mucous membranes?

Hep B needlestick?

Hep C needlestick?

A

.3%

.09%

37-62% for hep B with 22 to 31% developing clinical Hepatitis B infection following needlestick.

.5 to 1.8% risk of transmission.

205
Q

True or False: Under HIPAA a provider does not need consent from a patient to communicate HIPAA protected information to other treating providers?

A

True.

206
Q

When is infromed consent for an elective procedure best obtained?

A

Best obtained by the physician in the office/clinic setting a few days before the scheduled procedure.

207
Q

What is the order of next of kin for making medical decisions or obtaining consent?

A

Spouse, then children (in no particular order), parents, siblings, and then grandchildren.

208
Q

How is emergent consent obtained in absence of legal consent for the following situations:

Life threatening surgery?

Non-life threatening injury?

A

Surgeon should confirm and document the necessity of care with a fellow orthopaedic surgeon or colleague.

Consent must be obtained prior to intervention in cases of non-life threatening injuries.

209
Q

How can wrong site surgery best be avoided?

A

By involving the patient in identifying correct side or site in the pre-operative area and prior to induction.

Displayin pertinent imaging in the operating room

Marking the correct site with the surgeon’s initials visibly in the surgical field.

Performing a time-out with the operating room team prior to incision.

210
Q

According to JCAHO what should be included in the surgical “time-out?”

A

Identify the correct side, site, and patient

Verify the correct procedure.

All members of the team should be present for the time out.

Surgeon is most effective OR team member at reducing complications when using surgical check list and “time-out”

211
Q

What is the most common clinical diagnosis associated with orthopaedic lawsuits?

A
  1. Osteoarthritis (21%)
  2. Disorder of joint, not including arthritis
  3. Fracture of femur

The most commonly associated operative procedure is those on joint structures not including spinal fusion.

212
Q

What is the physician payments sunshine act 2010?

A

Requires collection and reporting of financial relationships between physicians / teaching hospitals and businesses (manufacturers of drugs, devices, and medical supplies).

All payments beyond $10 must be reported to Centers for Medicare and Medicaid Services

213
Q

Does a second opinion surgeon have a legal obligation to disclose if the standard of care has been breached by a treating physician?

A

No, he does not have a legal obligation.

He has an ethical obligation.

214
Q

What four elements must be alleged and proven in a court of law for a succesful patient-plaintiff lawsuit for medical negligence?

A

DUTY- The duty of the physician is to provide care equal to the same standard of care ordinarily exectued by surgeons in the same medical specialty.

BREACH OF DUTY- Breach of duty occurs when action or failure to act deviates from the standard of care.

CAUSATION- causation is present when it is demonstrated that failure to meet the standard of care was the direct cause of the patients injuries.

DAMAGES- Damages are monies awarded as compensation for injuries sustained as the result of medical negligence.

215
Q

Does a worker compensation patient have the ability to choose their own physician?

A

It depends upon the state statutes.

216
Q

What is the difference between impairment and disability in the worker compensation realm?

A

IMPAIRMENT: loss of function resulting from an anatomic or physiologic derangement.

DISABILITY: Limitation of an individual’s capacity to meet certain personal, social, or occupational demands.

217
Q

List some of the acceptable stnadards of professionalism regarding relations with industry and hospitals?

A

Practicing orthopaedic surgeons may accept tuition, travel, and modes hospitality (including meals and receptions) to attend an industry sponsored non-CME course given at a local convention center.

Must disclose relationships with industry to patients, colleagues, and their institution

Can only receive gifts with a market value under $100

No direct kick-back can be given to a physician from industry or hospital systems

218
Q

What are Stark II Laws?

A

Physicians cannot refer patients to centers in which they have a financial interest.

219
Q

Can patients family members act as translators?

A

Only if the patient offers or agrees.

220
Q

What is EMTALA?

A

The emergency medical treatment and active labor act.

Patient can be transferred when:

There has been formal acceptance by the accepting facility.

The benefits of transfer must outweigh the risks.

The exiting facility must not have the resources to properly handle that particular patient and/or situation.

221
Q

What are the three phases of the WHO surgical checklist?

A
  1. The sign in (before induction)
  2. The time out (before skin incision)
  3. The sign out (before the patient leaves the room)
222
Q

Implementation of a surgical safety checklist has been shown improvements in?

A

Surgical mortality

In hospital complications

Adherence to surgical plan in OR crisis situations (e.g., massive hemorrhage, cardiac arrest)

223
Q

What is included in the before induction of anaesthesia WHO checklist?

A
224
Q

What is included in the before skin incision WHO surgical checklist?

A

Serve as a guideline. Additions and modifications can be made.

225
Q

What is included in the before patient leaves operating room WHO surgical checklist?

A
226
Q

What is ICD-10?

A

International Classification of Disease-10 (ICD-10)

Developed by the WHO

alphanumeric seven-digit code

Allows description of chonicity, phase of care, effects, and laterality.

227
Q

What constitutes a consutation for billing?

A

Service requested by another physician

Advice must be the object of the request, not a transfer of care

A request must be documented in the chart

Level of visit must be documented

Written response to requesting physician must be provided by consulting physician.

228
Q

What are th known 2-digit code billing modifiers.

A
229
Q

What is and is not included in the global period?

A

WHAT IS INCLUDED: Preoperative visits and work, OR Preparation, skin to skin work, application of immobilization in the OR. Postoperative care inpatient and subsequent office visits for up to 90 days.

WHAT IS NOT INCLUDED:

Visits for separate problems, evaluation by physician that is part of a different group, return trip to the operating room for complication from initial procedure, application of immobilization outside of the OR, diagnostic tests and procedures, staged procedures and visits outside of 90 days (some procedures do have a shorter global period than 90 days.)

230
Q

When do most children develop hand dominance?

A

During their third year of life.

Strong hand preference in a child younger than age 2 may indicate a neurologicla deficit.

persistence of ambidexterity is not pathological.

231
Q

What is the orthopaedic diagnosis most likely to result in a successful malpractice claim?

A

Fasciotomy or compartemnt syndrome related cases.

Fractures are the most common cause of malpractice suits while arthroplasty is currently #2.

232
Q

Describe some of the common orthopaedic conditions that occur at the various zones of the physis?

A
233
Q

What is a normal value for a timed get up and go test?

A

< 12 seconds in normal in a population of adults of all ages.

> 26 seconds in predictive of persistent use of ambulatory aids

234
Q

What is the best method to measure limb-length discrepancy in a patient with a knee flexion contracture?

A

Obtain a lateral CT scanogram

235
Q

What osteotomy is generally recommended for a valgus knee?

What about a varus knee?

A

DFO for a valgus knee. Defomrity is at lateral femoral condyle. HTO will lead to joint line obliquity.

HTO for a varus knee.

236
Q

What is a normal ICP?

A

normal range for intracranial pressure is 5-15 mmHg

237
Q

Briefly explain the following:

Cost-benefit analysis

Cost-effectiveness analysis

Cost-utility analysis

Decision analysis

A

Cost-benefit anlaysis- conversion of effects into the same monetary terms as the costs and compates them.

Cost-effectiveness anlaysis- conversion of effects into health terms and describes the costs for some additional health gain (eg, cost per additional event prevented).

Cost-utility analysis- conversion of effects into personal preferences (or utilities) and describes how much it costs for some additional quality gain (eg, cost per additional quality-adjusted life-year).

Decision analysis- application of explicit, quantitative methods to analyze decisions under conditions of uncertainty.

238
Q

What is the most common complication after an interscalene block?

A

Sensory neuropathy

239
Q

When should bone mineral density be performed for women?

A

Women age 65 years or older.

Postmenopausal women with at least one risk factor for osteoporotic fractures: prior fragility fracture, low estrogen levels, premature menopause, long-term secondary amenorrhea, glucocorticoid therapy, maternal history of hip fracture, or low body mass index.

240
Q

Describe the ICD-10 code format?

A

consists of 3-7 characters

1st is alpha, the 2nd is numeric, and the 3rd-7th are alpha or numeric.

The seventh charcter corresponds to phase of treatment.

241
Q

Describe some of the common gait problems with prosthesis and how to trouble shoot them.

A
242
Q

Major Factors that increase risk for venous thromboembolism?

A

Previous VTE

Obesity

Type of surgery (such as TJA)

Hypercoagulable states, MI, and CHF

Family history of VTE

Hormonal replacement therapy

243
Q

What percentage of bone mineral has to be lost before plain radiographs will accurately demonstrate the loss?

A

40%

244
Q

What is meralgia paresthetica?

A

Lateral femoral cutaneous nerve entrapment.

Can be caused by prolonged hip flexion and tight belts.

Can also occur after being prone for long spine procedures

TX is removal of compressive objects, therapy, and NSAIDS. Almost always resolves with this and time.

245
Q

What are indications for hyperbaric oxygen treatment?

What are contraindications to hyperbaric oxygen treatment?

A

Crush injury, wound healing, and early compartment syndrome

COPD -> bleb formation that risks pneumothorax

History of Bleomycin treatment -> pneumonitis

Pneumothorax

Insulin pump which can malfunction under pressure

246
Q

What is the recommended antibiotic to treat cutibacterium acnes infections?

A

formerly known as Propionibacterium acnes.

Penicillin is best

Can also use piperacillin, tazobactam, and vancomycin.

ABOS1 (13 decks)

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