General Orthopaedics Flashcards

1
Q

Most likely metal to experience crevice corrosion?

A

316L Stainless steel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Metal with highest risk of galvanic corrosion?

A

316L stainless steel and Co:Cr alloy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How to reduce metal corrosion?

A

Use similar metals and plates
Passivation (coat metal)

Titanium alloy undergoes self-passivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Types of corrosion

A

1) Galvanic
2) Crevice
3) Pitting
4) Stress
5) Fretting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Labs to get with thumb hypoplasia?

A

CBC (Fanconi anemia)

Chromosomal challenge test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Parona’s space?

A

Potential space of communication between small finger and thumb - lies between fascia of PQ and FDP conjoined tendon sheaths.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of Nerve injury?

A

Neuropraxia (Sunderland 1st) - focal demyelination (no fibrillation on EMG)

Anonotmesis (Sunderland 2nd degree) - conduction block and Wallerian degeneration. Endoneurium intact.

Neurotmesis - disruption of endoneurium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Latency and velocities seen in CTS?

A
Distal sensory latency > 3.2ms
Motor latency > 4.3ms
Velocity < 52m/sec
Motor action potential decreases
Sensory nerve action potential decreases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How to differentiate TAR from radial clubhand?

A

TAR (AR) - thrombocytopenia and absent radius - typically has thumb present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Medial talar dome vs. lateral talar dome OCD lesions

A

Medial talar dome - more common, posterior, larger/deeper, no trauma.

Lateral talar dome - trauma, superficial, central or anterior, lower healing rates, more symptomatic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pathophysiology of dupuytrens disease

A

Myofibroblast is dominant cell type - actin along long axis and extracellular fibronectin

Type III collagen predominates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is not invloved in Dypuytren’s disease?

A

Cleland’s ligament and transverse ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Dexa Scan Measurements?

A

BMD: absolute scores from Lumbar spine and hip
T-Score: BMD relative to young women (30 yo)
Z-Score: BMD relative to similar aged patients
Osteopenia: L2-L4 density 1 - 2.5 SD below T-score
Osteoporosis: L2-4 density > 2.5 SD below T-score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Biologics to to be used on osteoporosis?

A

Raloxifene - SERM (dont use if hx DVT)

Teriparatide (Forteo) - 1-34 amino terminal residues of parathyroid hormone, activates osteoblasts. Osteosarcoma risk in Pagets disease.

Denosumab (Prolia) - Ig2 against RANKL, don’t use longer than 2 years. Continuous infusion causes resorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mnemonic for bisphosphonates?

A

PRAZI-N and TEC-No

Pamidronate, Risedronate, Alendronate, Zolendronate, Ibanddronate - Nitrogen containing (inhibit farnesyl pyrophosphate synthase which is a mavelonate pathway to ultimately inhibit small GTPases)

Tiludronate, Etidronate, Clodronate - Non-nitrogen containing (Toxic ATP analog)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Vitamin D and Calcium dosing recommendations?

A

1200-1500mg Calcium and 400-800 IU Vit D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pharmacologic agents in osteoporosis?

A
Calcium/Vitamin D
Bisphosphonates (PRAZI-N and TEC-No)
HRT
Estrogen Replacement
Calcitonin - reduce bone pain in osteoporotic fractures, binds to osteoclasts to inhibit
Raloxifene (Evista) - SREM
Teriparatide (Forteo) - 1-34 amino terminal of PTH
Denosumab (Prolia) - anti RANK-L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Types of Bone mineralization disorders

A

1) Vitamin D Resistant Rickets (Hypophosphatemic) - XLD
2) Vitamin D Deficiency Rickets (Nutritional)
3) Type I Vitamin D Dependent - AR
4) Type II Vitamin D Dependent - AR
5) Hypophosphatasia - AR
6) Renal Osteodystrophy High Turnover - Renal Dx
7) Renal Osteodystrophy Low Turnover - Renal Dx
8) Hyperparathyroidism - 90% adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathophysiology of Renal Osteodystrophy?

A

Low Ca, high phos, refractory high PTH, high alk Phos

Hypocalcemia - inability of kidney to convert vit D3 (25-OH Vit D3) to calcitriol by 1alpha-hydroxylase due to hyperphosphatemia. Results in insoluble CaPO4 to form and remove from circulation.

Hyperparathyroidism and Secondary Hyperphosphatemia - caused by hypocalcemia and lack of phosphate excretion.

Uremia related phosphate retention.

Complications - genu Valgum and B/L SCFE (Secondary spongiosa of metaphysis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Labs in metabolic bone disease?

A
Calcium
Phosphorus
Alk Phos
PTH
Vitamin D - 25(OH) Vitamin D
1,25(OH) Vitamin D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Metabolic bone diseases with Elevated calcium?

A

Hypophosphatasia

Hyperparathyroidism

All others are low or low normal (Nutritional Rickets)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Metabolic Bone diseases with elevated phosphate?

A

Hypophosphatasia

Renal Osteodystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Metabolic Bone diseases with decreased alkaline phosphatase?

A

Hypophosphatasia

All others elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Metabolic Bone diseases with elevated PTH?

A
All with the exception of 
low turnover renal osteodystrophy
Vit D resistant rickets
Type II Vit D dependent
Hypophosphatasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Type 1 vs Type 2 Vitamin D dependent metabolic bone disease?

A

Type I has decreased 1,25(OH) Vit D - missing enzyme in proximal tubule of kidney (1-alpha-hydroxylase)

Type II has INCREASED 1,25(OH) Vit D - missing receptor for 1,25(OH) Vit D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

High turn over renal bone disease vs. Low turnover renal bone disease

A

High turnover bone disease - secondary hyper PTH - Hyperphosphatemia lowers serum Ca, stimulates PTH results in bone resorption

Low turnover bone disease - No secondary hyper PTH
- Normal PTH levels - you get aluminum deposition into bone mineralization that impairs osteoblast proliferation and PTH release from PTH gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Regulators of Ca and Phosphate metabolism

A

PTH - Chief cells of parathyroid glands

1,25(OH) Vitamin D - proximal tubule of kidney

Calcitonin - parafollicular cells of thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Actions of parathyroid Hormone?

A

Decreased Ca levels cause release
Increased Ca and 1,25(OH) Vit D inhibit release

Results in increased Ca level and decreased Phosphate (phosphate thrashing hormone).

Kidney: Stimulates 1-alpha-hydroxylase to make active vitamin D, increase resorption of Ca, urinary excretion of Phosphorus

Bone: Direct cAMP mediated osteoclastic resorption of bone

Intestine: No direct effect, increased active Vitamin D results in increased absorption of Ca and P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Actions of 1,25(OH) Vitamin D

A

Stimulates intestinal resorption of Ca and P
Stimulates Osteoclastic resorption of bone

Results in increased Ca and P levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Action of calcitonin?

A

From parafollicular cells of thyroid

Stimulated by elevated Ca levels

Inhibits osteoclastic resorption of bone (direct)

Results in decreased Ca levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is rickets?

A

Defect in mineralization of osteoid matrix due to inadequate calcium and phosphate

Prior to physeal closure called Rickets
After physeal closure called osteomalacia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Most common form of rickets?

A

Familial Hypophosphatemic Rickets (Vitamin D resistant Rickets)

  • X Linked Dominant - PHEX gene
  • inability of tubules to resorb phosphate, results in high phosphate in urine
  • Low Phosphate and elevated alk phos. Normal PTH, Ca, Vitamin D.
  • Triad of hypophosphatemia, short, lower limb deformities.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What zone of physis is widened in Rickets?

A

Hypertrophic zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Nutritional vs. hypophosphatemic rickets?

A

Nutritional - low vitamin D levels is primary problem so there are low-norm Ca levels, low phos, high alk phos, and increased PTH levels - Tx vitamin D

Hypophosphatemic - XLD (PHEX gene) - low phosphate resorption and near normal Ca levels results in normal PTH levels, Tx with VitD and Phos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Mechanism of Factor V Leiden thrombophilia?

A

Altered Factor V cannot be inhibited by protein C. Thus Factor V (co-factor for Factor Xa) binds to Factor Xa to produce high amounts of thrombin and drive clotting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Hypercoagulable disorders?

A
MTHFR/C677 gene (highest risk)
factor V Leiden
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Activated protein C resistance

(M,3,5,C,S)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Brief overview of clotting cascade

A
Intrinsic Pathway - XII, XI, IX
Extrinsic pathway (endothelial damage) VII activated by TF (thromboplastin)

Factor X to Xa activates Factor II (prothrombin) to Factor IIa (thrombin) which activates factor I (Fibrinogen) to Factor Ia (fibrin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Mechanism of Heparin?

A

Binds and activates antithrombin III to inhibit factors IIa, IIIm and Xa.

Subcutaneous version is unfractionated heparin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is fractionated heparin and mechanism of action?

A

Also known as low molecular weight heparin - enoxaparin (Lovenox) or Dalteparin

Several sites but main is inhibits Factor Xa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Direct factor Xa inhibitors?

A

Rivaroxaban (Xarelto)
Apixaban (Eliquis)
Edoxaban (Savaysa)

Metabolized in Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Indirect Xa inhibitors?

A

Fondaparinux (Arixtra)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Coumadin mechanism?

A
Affects extrinsic clotting pathway and Vitamin K 
dependent factors (II, VII, IX, X)

Inhibits vitamin K 2,3 epoxide reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Direct thrombin inhibitor?

A

Thrombin = Factor IIa

Dabigatran (Pradaxa) - Metabolized in kidney

Argatroban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Mechanism of TXA?

A

Antifibrinolytic that promotes and stabilizes clot formation

Competitively inhibits activation of plasminogen and binds lysine binding site. Plasmin breaks down fibrin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Antiplatelet agents?

A

Aspirin (acetylsalicylic acid) - inhibits prostaglandins and thromboxanes (causes platelet aggregation).

Clopidogrel (Plavix) - binds ADP receptor on platelet to activate GPIIb/IIIa complex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Mechanism of penicillins?

A

Bactericidal - blocks cross linking via competitive inhibition of the transpeptidase enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Carbapenems

A

Imipenem
Meropenem
Doripenem
Ertapenem

Broadest activity - no MRSA or mycoplasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Abx that bind 30S ribosomal subunit?

A

Aminoglycosides - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

Tetracyclines - Tetracycline, Doxycycline, Minocycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Aminoglycosides and mechanism of action?

A

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

Bactericidal - irreversible binding to 30S

Aerobic gram-negatives, enterobacter, pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Tetracyclines and mechanism of action?

A

Tetracycline
Doxycycline
Minocycline

Bacterostatic - blocks tRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Abx that bind 50S subunit?

A

Macrolides (erythromycin, azithromycin, clarithromycin)

Chloramphenicol

Lincosamides (Clindamycin) - inbibits peptidyl transferase by interfering with amino acyl-tRNA complex

Linezolid

Streptogramins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Abx that interfere with DNA synthesis?

A

Fluoroquinolones - Ciprofloxacin, Norfloxacin, Levofloxacin

Metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Floroquinilones and mechanism of action?

A

Ciprofloxacin, Norfloxacin, Levofloxacin

4th generation: moxifloxacin, gemifloxacin

Inhibit DNA gyrase

Achilles tendon rupture, impaired fracture healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Mechanism of rifampin?

A

Inhibits RNA transcription by inhibiting RNA polymerase (DNA dependent RNA polymerase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Definition of sensitivity?

A

Probability that test results will be positive in patients with the disease

Detects disease! True positive.

A/(A+C)

Remember: set up 4x4 table with Test on left and Disease on top. A (upper left), B (upper right), C (lower left), D lower right.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Definition of specificity

A

Probability that test results will be negative in patients without the disease.

Detects Health!! True Negative.

D/(D+B)

Remember: set up 4x4 table with Test on left and Disease on top. A (upper left), B (upper right), C (lower left), D lower right.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Definition of positive predictive value?

A

Probability a patient with positive test will have the disease.

A/(A+B)

Remember: set up 4x4 table with Test on left and Disease on top. A (upper left), B (upper right), C (lower left), D lower right.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Definition of negative predictive value?

A

Probability a patient with a negative test will not have the disease.

D/(D+C)

Remember: set up 4x4 table with Test on left and Disease on top. A (upper left), B (upper right), C (lower left), D lower right.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Likelihood ratio?

A

Likelihood a given test result will be expected in a patient with the target disorder

Positive likelihood (Chances of a disease is changed by a positive rest) = Sensitivity /(1-Specificity)

Negative likelihood = (1-Sensitivity)/Specificity`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Relative Risk Definition.

A

Risk of developing disease for people with known exposure compared to risk of developing disease without exposure

= Incidence of exposure/incidence of no exposure.

  • This is basically incidence (incidence in exposed/risk in unexposed). And a prospective cohort study design is the only type to calculate incidence.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Odds ratio definition?

A

Represents the odds that an outcome will occur given a particular exposure, compared to the odds that the outcome will occur without the exposure

= (axd)/bxc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Where are odds ratios calculated from?

A

From case control studies (retrospective)

From logistic regression models

Odds ratios approximate RR when outcome is rare (<10%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Number needed to treat definition?

A

Number of patients needed to treat to get favorable outcome.

NNT = 1/ARR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Type 1 vs Type 2 error

A

Type I Error: Reject null hypothesis even though true, alpha error set to 0.05

Type II Error: Accept null hypothesis even though false (Beta usually 0.2) Power = 1-Beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is a bonferroni correction?

A

Post-Hoc correction made to P values when several dependent or independent statistical tests are being performed simultaneously on a single data set.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Parametric data vs. non-parametric data?

A

Parametric: normally distributed

Non-parametric: Not normally distributed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Continuous data tests?

A

Parametric

  • Two Groups (Paired) - Dependent (paired) t-test
  • Two Groups (Unpaired) - Independent t-test
  • Three or more - ANOVA

Non-parametric

  • Two Groups (Paired) - Wilcoxon Rank-Sum Test
  • Two Groups (Unpaired) - Mann-Whitney U Test
  • Three or more - Kruskal-Wallis Test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Categorical Data Tests?

A

Parametric/Nonparametric

  • Two or more variables: Chi Square
  • Two or more variables (Small sample size): Fisher’s exact test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is a funnel plot used for?

A

Scatter plot of the intervention to detect bias in meta-analysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Design of the ROC curve?

A

X-axis: False positive rate (1-specificity)

Y-axis: True positive rate (sensitivity)

Area under the curve - used to compare different tests, higher c-statistics mean better test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Levels of Evidence?

A

Level 1: RCT, Meta-analysis

Level 2: Bad RCT (F/u <80%), Prospective cohort study, meta-analysis of level II

Level 3: Retrospective cohort study, case-control study, meta-analysis of level III

Level 4: Case series

Level 5: Case report, opinion, observation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is a prospective cohort study?

A

Groups separated non-randomly into treatment groups and followed/compared. Exposure occurs after initiation of study.

Analysis reported as relative-risk

Level II evidence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is a case control study?

A

Groups are separated by presence or absence of disease and examined for the prior exposure of interest.

Analysis reported as odds-ratio

Level III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Most common clinical study type in orthopaedics?

A

Level 4 (retrospective case series)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Hereditary neuropathies?

A

Friedreich Ataxia - AR disorder, cardiomyopathy and cavus foot, scoliosis

Charcot Marie Tooth - AD, myelin degeneration (PMP22 on Chr 17), Pes cavus from Tib ant and P brevis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Anterior horn cell disorders

A

Spinal Muscular Atrophy (SMA) - AR with SMN gene lack of SMN-1 protein

Type 1 (Acute Werdnig Hoffman) - <6mo, no DTR, tongue fasciculations

Type II (Chronic WH) - 6-24 months may live to 40s

Type III (Kugelberg Welander) - 2-10 years, walk as children

Treat hip subluxation non-op

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Causes of limb length discrepancies?

A

Congenital - PFFD, fibular deficiency, hemihypertrophy, DDH

Paralytic - CP, Polio

Infection, tumors, trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Angle in infantile blount disease?

A

Drennan metaphyseal-diaphyseal angle > 16 deg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Treatment of infantile blount disease?

A

If <3 years and stage I or II brace

Stage II and III proximal osteotomy

Higher stage need something crazy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Types of tibial bowing?

A

Posteromedial - probably mild, calcaneovalgus foot, will develop LLD (3-4cm)

Anteromedial - fibular hemimelia, equinovarus foot, assoc with coxa vara and PFFD, tarsal coalition and ball and socket ankle joint

Anterolateral - congenital pseudoarthrosis, NF, brace to prevent fx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Gene associated with clubfoot mutation?

A

PITX1 mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Deformity associated with club foot?

A

Cavus (tight intrinsics, FHL, FDL)

Adductus of forefoot (tight tibialis posterior)

Varus (tight tendoachilles, tibialis posterior, tibialis anterior)

Equinus (tight tendoachilles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Most common types of tarsal coalitions?

A

Calcaneonavicular

Talocalcaneal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

AIS MRI Indications?

A
Left thoracic curves
Pain
Apical Kyphosis
Rapid curve progression
Neurologic signs (abdominal reflexes)
Congenital anomalies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Factors affecting AIS progression?

A

Skeletal maturity - Risser sign, hand digit physes

Peak growth velocity - Prior to menarche, occurs prior to Risser 1, tri-radiate cartilage

Curve magnitude > 20 deg

Curve Type Thoracic>Lumbar and Double>Single

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Scoliosis progression after maturity?

A

Thoracic > 50
Lumbar >30
1-2 deg per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Treatment of AIS?

A

<25 deg and immature - observe
< 40 and mature - observe
25-40 deg and immature - brace
>50 - surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Measurement in early onset scoliosis?

A

RVAD - rib vertebral angle difference (Mheta)

> 20 has high risk for progression

RVAD = Concave - Convex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Congenital scoliosis with worst prognosis?

A

Unilateral bar with contralateral hemivertebrae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Measurement in congenital coxa vara?

A

Hilgenreiner-Physeal line - should be < 25 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Classification for Legg-Calve-Perthes Disease?

A

Lateral pillar classification - only at the end of fragmentation phase.

A = none
B = <50% loss of height
B/C border - lateral pillar narrowed with height 50%
C = >50% loss of height

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Prognosis in Legg-Calve-Perthes Disease

A

Worse if 6 and older and if total head involvement

Good outcome is good ROM and spherical head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Differentiation between multiple epiphyseal dysplasia and Spondyloepiphyseal dysplasia?

A

MED - autosomal dominant, COMP gene mutation, spine is normal, disproportionate dwarfism

SED - AD, Mutation on chromosome 12 (COL2A1), proportionate, spine involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Features and genetics of Diastrophic dysplasia?

A

Genetics - DTD gene (Chr 5), sulfate transporter protein results in undersulfation of proteoglycans, autosomal recessive

Features - short, cauliflower ears, hitch hikers thumb, fused PIPJs, severe club feet, kyphosis and scoliosis

Cervical kyphosis severe, quadriplegia a risk, urgent management required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Composition of bone?

A

40% Organic - Collagen (resistes tensile forces), proteoglycan (resists compressive forces), matrix protein

60% Non-organic - Hydroxyapatite (resists compression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Composition of hydroxyapatite?

A

Ca10(PO4)6(OH)2

Resists compression!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Defect in Osteopetrosis?

A

Osteoclast malfunction - Carbonic anhydrase defect, OPG over expression, get decreased remodeling

Ruger jersey spine and erlenmyer femur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Pynknodysostosis

A

Cathepsin K deficiency

Casuses acro-osteolysis of terminal phalanges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Sclerosteosis

A

Sclerostin deficiency

Increased WNT/B-catenin and increased osteoblast activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Function of sclerostin and dickkoph-1 (Dkk-1)

A

Direct inhibitors of Wnt/B-catenin pathway (activates osteoblasts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Chondroblast promoting conditions and growth factors?

A

hMSC in medium strain and low O2 conditions and in presence of SOX-9

Growth Factors (TIP) - TGF-B, IGF-1, PDGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Function of chondrocytes?

A

Produce cartilage (collagen and PG)

From chondroblasts in the superficial/tangential layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What gives cartilage compressive strength?

Composition of proteoglycan aggregate?

A

Proteoglycans (hydrophilic)

Keratin sulfate and chondroitin sulfate bind to protein core and chains are linked together on a hyaluronic acid backbone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Cartilage changes in osteoarthritis?

A

H2O increases while collagen and quantity decrease

Decreased x-linking and lower modulus

Chondrocyte number unchanged

Increased IL1, IL6, and TNFa. Collagenase/MMPs degrade collagen and stromelysin degrades PG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Cartilage changes in aging?

A

Old and stiff…

H2O decreases, collagen quantity unchanged

Stiffer collagen (increased x-linking and diameter)

Proteoglycan: increased keratin sulfate and decreased chondroitin sulfate.

Decreased chondrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Intervertebral disc composition?

A

85% water, PG, collagen 1 and II

Nucleus pulposus

  • high PG, low Col
  • Type II collagen
  • Compressive strength

Annulus Fibrosis

  • Low PG and high Collagen
  • Type I collagen
  • Tensile strength
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Changes seen in an aging disc?

A

Decreased H2O and decreased PG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Protein specific to ligaments?

A

Elastin

Also has type I collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What type of collagen dominates in ligament healing?

A

Type III Collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Changes in a healed ligament?

A

Increased number of fibers but lower x-linking, diameter, and mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Protein that regulates tendon diameter?

A

Decorin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

When are tendon repairs weakest?

A

During inflammatory phase (7-10 days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

In early OA what collagen type increases?

A

Type X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Diseases in reserve zone?

A

PKGD - matrix production

Pseudoachondroplasia (COMP gene)
Kneist syndrome (Col 2A1 gene)
Gaugher Disease (B-glucocerebrosidase)
Diastrophic dysplasia (AR, DTDST sulfate transport gene)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Diseases in the proliferative zone?

A

Cellular division

MEGA

MHE (AD, EXT 1, 2, 3)
Gigantism
Achondroplasia (AD, FGFR3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Diseases in the Hypertrophic Zone?

A

Cellular hypertrophy - longitudinal growth

3 Ss

SCFE
SH Fx
Schmid

Nutritional rickets (ZPC)

Zone of provisional calcification involves Col X and is the last to calcify

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Pathology of lead poisoning?

A

PTHrP regulates (inhibits) physeal maturation in the hypertrophic zone

Lead inhibits PTHrP and leads to accelerated maturation of bone at an earlier age (decreased peak BMD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Diseases in the metaphysis of the growth plate?

A

Primary Spongiosa - woven bone - Corner Fx

Secondary spongiosa - lamellar bone - Endocrine SCFE and Renal osteodystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Appositional growth of the growth plate?

A

Zone of Ranvier - fibrous ring from epiphysis to the diaphysis

Perichondral ring of Lacroix - contributes to physeal strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Limb Embryology - Growth patterns

A

AER - proximal to distal (interdigital apoptosis) - FGF growth factor
ZPA - radial to ulnar - Shh gene
WNT - dorsal to ventral - Wnt (Wings on your dorsal surface)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Renal osteodystrophy knee deformity?

A

Genu valgum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Most common disorder of bone mineralization, genetics, mechanism, labs, treatment?

A

X-linked hypophosphatemic rickets (Vitamin D dependent), XLD - PHEX gene

Inability to resorb phosphate in the kidney

Low phos - everything else normal (Normal Ca, PTH, and Vitamin D)

Treat with phosphate and vitamin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Hypercoaguable states?

A
M, 3, 5, C, S
MTHFR Gene
AT3 Deficiency
Factor V Leiden 
Protein C and S deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Osteoblasts derived from?

A

Mesenchymal stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Transcription factors directing cells down osteoblast lineage?

A

RUNX2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Function of osteoblasts?

A

Form Bone

Regulate osteoclast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What causes a cell in the Osteoblast lineage to become an osteoblast?

A

Low strain, high O2 environment

BMP/SMAD (Ser-Thr)
Core binding factor a1 (Cbfa1)/RUNX-2
WNT/B-catenin
PDGF
IHH/IGF-2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Osteoblasts produce what?

A
Alkaline phosphatase
Osteocalcin
Type I collagen
Bone sialoprotein
RANKL
Osteoprotegrin (binds RANK to decrease activity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Osteoblast activity is stimulated by what?

A

Intermittent PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Functions of Wnt proteins?

A

Promote osteoblast survival and proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What can sequester Wnts?

A

Sclerostin (Scl) and dickkoph related protein 1 (dkk1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Osteocytes are from what?

A

Former osteoblasts that are now enclosed in bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Receptors on osteoblasts

A
PTH - pulsatile = more bone, constant = resorption
1,25 Vit D
Glucocorticoids (decrease activity)
Prostaglandins (decrease activity)
Estrogen (increase activity)
134
Q

Receptors on osteoclast?

A

Calcitonin - inhibits osteoclast function

135
Q

Osteoclasts Make what in howships lacunae?

A

MMP
Cathepsin K
TRAP

136
Q

How do osteoclasts bind to site for resorbtion?

A

aVB3 on osteoclasts bind vitronectin (on bone) via the RGD sequence (arginine-glycine-aspartate).

137
Q

How do osteoblasts activate and downregulate osteoclasts

A

RANK-L production

Osteoprotegrin (OPG) - RANK receptor decoy and sequestors RANKL

138
Q

What activates osteoclasts?

A

Inflammatory environment - IL-1, IL-6, TNF-a, PG-E2

VitD, PTH, PTHrP receptors on osteoblast cause increase in RANKL to activate osteoblast.

139
Q

What inhibits osteoclasts?

A

Calcitonin (Direct inhibitor of osteoclasts), TGF-B, IL-10.

OPG and Estrogen (indirectly via OB/RANKL)

140
Q

Function of osteocytes?

A

Detect strain and regulate bone

Produce sclerostin and communicate via canaliculi

141
Q

How does sclerostin function?

A

Functions through the DKK-1 (dikkoph pathway) which decreases the WNT/B-catenin pathway to decrease osteoblast activity.

142
Q

Defect in cleidocranial dysplasia

A

Autosomal dominant defect in CBFA-1/RUNx-2 results in defect in intramembranous ossification

Missing clavicles and teeth.

143
Q

Types of collagen and defects?

A

Collagen I - BONEs, ligaments, tendons - OI

Col II - Cartilage - Dx SED and Kniest syndrome

Col III - tendon/ligament healing - Dypuytrens

Col V - stabilizes col I

Col IX - stabilizes Col II - MED

Col X - initial fx healing - Schmid chondrodysplasia

Col XI - stabilizes all types of collagen - Stickler syndrome

144
Q

Proteoglycan composition and function?

A

Hydrophilic and give compressive strength

Keratin sulfate and chondroitin sulfate subunits bind on a protein core and are linked together on a hyaluronate backbone.

145
Q

Articular cartilage collagen arrangement?

A

Superficial (tangential zone) - top 10-20% - has the highest Collagen II and H2O - collagen fibers arranged tangential to surface

Middle transitional zone

Deep Zone - highest PG with fibers arranged perpendicular to surface. Tidemark zone has Collagen X.

146
Q

Key lubricating protein of synovial fluid?

A

Lubricin

147
Q

Cells that make synovial fluid?

A

Type A cells - macrophage-like

Type B cells - fibroblast like and produce synovial fluid (ultrafiltrate of plasma).

148
Q

Muscle fiber types?

A

Type 1 (slow twitch) - aerobic, high endurance, slow oxidative (first to be recruited)

Type 2A -

Type 2B - anaerobic, high speed, high strength, ATP-CP system

Force generated depends on orientation and cross sectional area of the muscle.

149
Q

Muscle Changes with exercise?

A

Increased collagen turnover but increase in NET collagen

Anaerobic increases functional motor units and cross sectional area

Aerobic increased capillary density

150
Q

Primary bone healing conditions

A

Low strain

No callus forms - intramembranous ossification and haversian/cutting cone remodeling.

151
Q

Findings of hyperparathyroidism?

A

Increased PTH (Ademona)

High Ca
Low Phos
High AlkPhos (OB upregulation)
Brown tumors from focal demineralization
Complications from Hyper Ca - stones, groans, moans, osteporosis, pancreatitis.
152
Q

Immune cell involved in metal allergy?

A

T cell mediated (Type IV)

153
Q

Rheumatoid arthritis serology?

A

RF+ - IgM against IgG
HLA DR4+
Anti-CCPa (most sensitive/specific)

154
Q

Cervical instability patterns in rheumatoid arthritis?

A

Atlanto-axial (ADI > 3.5mm flex/ex)
Basilar invagination (C2 cranial migration)
Subaxial subluxation

155
Q

Hypersensitivity reaction type from lupus?

A

Type III hypersensitivity (immune complex damage)

156
Q

Gout vs. pseudogout?

A

Gout - monosodium urate (Negative birefringence)

Pseudogout - calcium pyrophosphate dihydrate (Positive birefringence, blue rhomboids)

157
Q

Antibiotics that target cell wall?

A

B lactams - penicillins, cephalosporins

Vancomycin

Bacitracin (permeability)

158
Q

Antibiotics that target protein translation?

A

Macrolids (Clinda, azithro) - 50S

Aminoglycosides (Gent/Tobra - 30S (vestibular tox)

Tetracyclines (Doxy) - 30S

Linezolid - 70S (Serotonin syndrome)

159
Q

Which of the CC ligaments is stronger in the shoulder?

A

Conoid ligament stronger - more medial
Trapezoid more lateral

Acromial tip to CC ligament - 2.7cm

160
Q

Types of acromion?

A

Bigliani classification
Type I - flat
Type II - curved
Type III - hooked

161
Q

Types of os acromiale?

Most common type?

A

Pre-, Meso-, Meta-, Basi (From tip to origin)

Most common is junction between meso and meta

3-8% incidence

60% bilateral

162
Q

Primary blood supply of the humeral head?

A

Posterior humeral circumflex

Secondary - anterior humeral circumflex (anterolateral ascending branch aka the anterior irrigating branch) but does supply the proximal humerus and is disrupted 80% of the time.

163
Q

Divisions of the axillary artery?

A

Divided into 3 regions by the pec minor

Part I - Superior thoracic artery

Part II - Lateral thoracic trunk, Thoracoacromial trunk (ACDP)

Part III - anterior circumflex artery (terminates as the arcuate artery lateral to the intubercular groove), posterior humeral circumflex artery (supplies posterior greater tuberosity and head 64% of the time), subscapular artery (largest branch)

164
Q

Most important for stability of the SC joint?

A

Posterior SC capsule - true for anterior translation and posterior translation.

165
Q

Static stabilizers of the AC joint?

A

Capsule - superior/posterior capsule is most important for A-P stability

CC ligaments - Sup/inf translation

  • Trapezoid 16.7mm from joint and provides posterior restraint
  • Conoid - 35mm from joint provides superior restraint
166
Q

Borders and contents of the quadrilateral space?

A

Teres minor (superior), Teres Major (inf), long head of the triceps (medial), humerus (lateral)

Contains - posterior branch of the axillary nerve and the posterior humeral circumflex artery.

167
Q

Triangular Space vs. Triangular interval?

A

Triangular space - Teres minor, teres major and long head of the triceps (contains the scapular circumflex artery)

Triangular interval - teres major, long head of the triceps, humerus vs the lateral head of the triceps and contains the radial nerve and the profunda brachii artery.

168
Q

Branches off the brachial plexus cords?

A

Lateral - Lateral pectoral nerve

Posterior

  • Upper subscapular nerve, Thoracodorsal nerve, lower subscapular nerve
  • Axillary and radial nerve

Medial

  • Medial pectoral nerve
  • Medial brachial cuteaneous
  • Medial antebrachial cutaneous.
169
Q

How calculate on vs. off track?

A

Off track if HS > GT
On track if HS < GT

GT = 0.83(D)-d

D = largest diameter of the inferior glenoid. d = bone loss)

170
Q

Treatment of shoulder multidirectional instability

A

PT for at least 6 months.

Surgery is inferior capsular shift +/- closure of the rotator interval.

171
Q

Pathology found in internal impingement in throwers?

A

PASTA lesion (articular sided tear)
Tight posterior capsule and anterior microinstability
Posteriorsuperior labral tear during late cocking.

Contact of the articular rotator cuff with the posterosuperior rim of the glenoid labrum. internali

172
Q

Greatest tensile strength of the rotator cuff?

A

Bursal side (Greater tensile strength)

Articular sided - fails first.

Deceleration phase associated with tensile failure - posterior half of the supra and anterior half of the infra.

173
Q

Indications for operative repair of partial rotator cuff tears

A

Articular sided tears

  • > 6mm
  • > 50% thickness and tendon insertion

Bursal sided tears (more symptomatic and long healing time)
- >3mm

174
Q

History in a SLAP tear?

A

Pain (100%), clicking, dead arm, instability, weakness, decreased throwing velocity

Vague shoulder complaints in young person

175
Q

Types of SLAP tears and treatment

A

Snyder Classification
Type 1: degeneration and irregular surface

Type 2 - (MOST COMMON)
- Torn anterior to posterior

Type 3 - torn and detached from biceps (bucket handle tear)

Type 4 - Torn and propogated into the biceps tendon (<30% debridement, > 30% repair or tenodesis)

Types 1 and III - debride if anchor intact

Type 2 - repair vs. tenotomy/tenodesis

176
Q

ASIA Score?

A

A complete
B sensation, no motor, sacral sparing
C - Incomplete - motor function preserved below neurologic level with 1/2 muscles grade <3
D - Incomplete - motor function preserved below neurologic level with 1/2 muscles grade >3
E - Normal

Defined as most distal level > 3/5 given them next rostral level is 5/5.

177
Q

Brown Sequard sundrome

A

Hemitransection of cord

  • Ipsilateral loss of motor and proprioception
  • Contralateral pain and temperature loss

***Best prognosis

178
Q

Spinal imaging during frcture?

A

Once a fracture is identified imaging of the entire spine is recommended - 4.6-10% of non-contiguous spinal injuries.

179
Q

Radiographic diagnosis of occipitoatlantal instability?

A

Powers ratio BC/AO <1 (basion to posterior arch of C1)/(Anterior arch of C1 to opisthion)

Basion Dens interval <12

Orthosis treatment only if normal CT but positive MRI.

180
Q

Risk of type II odontoid non-union?

A
Initial displacement > 5mm (most important predictor of non-union)
>6mm translation
>10 deg angulation
Age > 50
Posterior displacement
181
Q

Hangmans fracture?

A

Bilateral pars fracture of C2

Type 1 - <3mm displacement, no angulation

Type II - >3mm traslation with significant angulation. Treatment is traction and halo

Type IIA - Significant angulation without translation. Tx extension and compression with halo. NO TRACTION.

Type III - translation, angulattion with uni or bilateral facet dislocation of C2-C3. High risk for neurologic injury.

182
Q

TLICS Scoring

A

Based on morphology, neurologic involvement, posterior ligamentous complex.

Morphology - Compression (1), burst (2), translational/Rotation (3), distraction (4)

Neurologic - normal (0), incomplete (3), complete (2), cauda (3)

PLC - intact (0), indeterminate (2), injured (3)

Nonsurgical <3, indeterminate 4, surgery >5

183
Q

AAOS recommendation for osteoporotic compression fractures

A

Strong - against vertebroplasty

Moderate - calcitonin for 4 weeks

Weak - bisphosphonate for prevention, L2 nerve block, kyphoplasty

Inconclusive - bed rest, herbal medicines, opioids, exercise, e-stim

184
Q

Brace for compression fracture?

A

Prospective, randomized clinical trial, Kim et al 2012 in JBJS.

At 12 weeks no difference in pain, disability, radiographic appearance, patient satisfaction with brace, soft brace, rigid brace.

185
Q

Components of the posterior spinal ligamentous complex?

A

Supraspinous ligament, interspinous ligament, ligamentum flavum, facet joint capsules.

186
Q

How is lauge-hansen classificaion used?

A

First is foot position and then second is force vector - example supination external rotation.

187
Q

Blood supply to the talus?

A

Artery of the tarsal canal (body)

Tarsal sinus (head)

Deltoid artery (body)

Dorsalis pedis artery (head)

188
Q

Talus fracture classification?

A

Hawkins

Type 1 - non displaced

Type II - fracture with subtalar dislocation

Type III - subtalar and ankle joint dislocation

Type IV - subtalar, ankle, and talar navicular joint dislocations.

189
Q

Factors that affect osteonecrosis after talus fracture?

A

Comminution p < 0.03

Open fracture p < 0.05

190
Q

What is the Hawkins sign and what does it predict?

A

Subchondral talar dome lucency - indicated presence of blood flow.

Best seen at 9 weeks

100% sensitivity (if you have it then no AVN), 57% specificity (if you dont have it then you still may not get AVN).

191
Q

Types of subtalar dislocation and blocks to reduction?

A

Lateral (15%) - navicular lateral to the talus - PT or EDL

Medial (85%) - ST more mobile in inversion - Navicular is medial to the talus. EDB or TN capsule can block.

192
Q

Blood supply to the femoral head?

A

Retinacular branches of the medial circumflex femoral.

193
Q

Acceptable closed reduction of tibial shaft fractures?

A

<1cm shortening
Angulation < 5-7 degrees
Rotational deformity < 10 deg

Intact fibula (varus deformity > 5deg is likely) and comminution are relative contraindications to closed treatment.

194
Q

Knee pain after tibial IMN?

A

10-60%

No difference with patellar tendon split vs parapatellar

Activity related and worse with kneeling

80% better with nail removal

195
Q

Adult flatfoot deformity classification

A

Stage 1 - tenosynovitis, SLHR intact, normal radiographs

Stage 2A - flexible, planovalgus foot, tenosynovitis, SLHR normal, mild too many toes sign, TN undercoverage < 40 deg

Stage 2B - Flexible, + too many toes, TN undercoverage > 40 deg, loss or Mearys angle

Stage 3 - Fixed deformity with degenerative changes

Stage 4 - valgus angulation of the talus and ankle and degenerative changes at the ankle.

196
Q

Treatment of PTTD

A

Stage 1 and 2 non-op

Stage 2B - FDL transfer, medial calc osteotomy, lateral column lengthening for TN undercoverage > 40%, possible cotton osteotomy (plantar flexion osteotomy of the medial cuneiform), +/- TAL

Stage 3 - triple fusion

Stage 4 - pantalar fusion

197
Q

Most common forms of tarsal coalition?

A

Talonavicular (excise if >50%) and calcaneonavicular (excise)

CT to diagnose

MRI to assess if painful

198
Q

Types of accessory navicular?

A

1 - sesamoid in PTT

2 - Synchondrosis with navicular (most common symptomatic type)

3 - Fused accessory

199
Q

When to do x-rays with bow legs?

A
Persistent varus at 2 years
Varus > 20 deg at any age
Short (<10th percentile)
Lateral thrust
Unusual diet
Family hx
200
Q

Assessment of xrays in bowed legs?

A

Tibio femoral angle
Mechanical axis
Metaphyseal-diaphyseal angle

201
Q

Langenskiold classification and the MD angle

A

Infantile blounts disease classification

1-2 - irregular metaphyseal ossification

3 - definite physeal deformity, fragmentation

4 - early bar formation

5 - profound physeal disruption

6 - severe articular disruption

Metaphyseal diaphyseal angle (Drennans) - <10 deg 95% physiologic. >16 deg 95% Blounts.

202
Q

Blounts disease non-operative treatment

A

Age < 2.5 and Langenskiold 1-2

Risk factors for non-op failure

  • Weight > 90%
  • Varus thrust
  • Age >3 years at brace initiation
  • Bilateral
  • Langenskiold III or higher
203
Q

Operative treatment of Blounts disease

A

Age >3, Langenskiold stage II-III, perform before age 4 to decrease risk of deformity and bar formation

Proximal tib-fib osteotomy and over-correct into 5-10 degrees of valgus, can also use guided growth.

Late onset - may need to correct multiple deformities (tibial varus, femoral varus, internal tibial torsion, increased posterior slope, LLD).

204
Q

LLD treatment guidelines

A

0-2cm - no tx
2-5cm - shoe lift, epiphysiodesis, shortening, lengthening
5-15cm - lengthening
>20cm - prosthetic fitting, amp.

205
Q

Association with hemi-hypertrophy?

A

Beckwith-Wiedemann syndrome

  • omphacele, neonatal hypoglycemia, macroglossia, embronyal tumors (Wilms tumor)
  • Sporadic vs AD vs chromosome 11
  • Get renal/abdominal ultrasound every 6 months until age 8 to screen for tumor or hepatoblastoma.
206
Q

Tibial deficiency treatment

A

Depends on quadriceps mechanism and presence of proximal tibia.

Amp if neither

Fibular centralization - need quad 3/5 and age <1 year, no fibular bowing.

207
Q

Focal femoral deficiency treatment?

A

Observation if bilateral
Lengthning - stable hip with femoral head, foot works, <20cm femur and >50% contralateral
Knee arthrodesis, syme amp - foot above knee level
Femur-pelvic fusion - no femoral head
Rotationplasty - foot at knee level, good ankle motion, no femoral head
Amputation/knee disarticulation - femur <50% of contralateral

208
Q

Types of tibial bowing

A

Anterolateral - think NF1 - prevent fractures with a clamshell brace. If fracture fix it.

Posteromedial bowing - probably mild. Associated with calcaneo valgus foot.

209
Q

Congenital knee dislocation differential

A

Syndromic - Larsens, myelodyaplasia, arthrogryposis, ehlers danlos

Non-syndromic - sporadic, abnormal positioning.

210
Q

Treatment of congenital knee dislocation?

A

Casting and splinting in flexion.

Pavlic for DDH

Surgery if <60 months flexion at 6 months - VY quads lengthening, release, k-wire/cast.

211
Q

Paprosky acetabular bone loss classification

A

1 - minimal bone loss - cavitary defect, kohlers line intact

Type 2 defects < 3cm migration
2A - Superior migration
2B - superolateral rim loss
2C - Medial wall and tear drop loss, kohlers line is violated, consider medial wall graft

Type 3 Defects have >3cm migration
3A - UP and OUT. Extensive rim and column loss and ischial lysis. 30-60% bone loss
3B - Pelvic discontunity with ischial bone loss. Up and In defect. >60% bone loss. Consider cup cage, triflange, pelvic distraction, augments.

212
Q

Paprosky femoral bone loss classification?

A

1 - minimal bone loss
2 - Extensive metaphyseal bone loss with intact diaphysis
3A - metaphyeal bone loss with 4cm diaphysis
3B - metaphyseal bone loss with less than 4cm bone diaphysis
4 - extensive metaphyseal bone loss and non-supportive diaphysis.

213
Q

L4 - S1 nerve root exam

A

S1 - Foot eversion (peroneal tendons), plantar flexion, toe walking, achilles reflex, lateral foot

L5 - EHL, no reflex, dorsum of the foot.

L4 - Tib ant, patellar tendon reflex, Medial foot border, quad

214
Q

C5 - T1 nerve root exam

A

C5 - biceps, deltoid, lateral arm, biceps reflex

C6 - wrist extension, lateral forearm, brachioradialis reflex

C7 - Triceps, wrist flexors, finger extension, triceps reflex, sensation to posterior arm and middle finger.

C8 - Interossi, finger flexors, no reflex, lateral forearm and hand sensation

T1 - Interossi, no reflex, medial arm sensation.

215
Q

Roots for iliohypogastric, ilioinguinal, LFCN, genitofemoral nerve, femoral nerve, obturator nerve, sciatic nerve.

A

Iliohypogastric and ilioinguinal - L1

Genitofemoral nerve - L1-2

LFCN - L2-3

Femoral nerve - L2, L3, L4

Obturator nerve - L2, L3, L4

Sciatic nerve - L4 to S2/3

216
Q

Vertebral artery anatomy?

A

Enters trasnverse foramen at C6 95% of time. Next most common is C5 followed by C7 then C4.

217
Q

Southwick neck landmarks?

A
Hardpalate - arch of the atlas
Hyoid bone - C3
Thyroid cartilage C4-5
Cricoid cartilage - C6
Carotid tubercle - C6
218
Q

Pneumonic for metastatic spine treatment considerations?

A
NOMS
Neurologic status
Oncological diagnosis
Mechanical stability
Systemic disease
219
Q

Cervical spine in down syndrome?

A

C1-2 instability in 15-25% screen by 5 years

ADI > 4.5mm - avoid stress across head/neck

ADI 10mm or neuro sx - stabilize

220
Q

Diastrophic dysplasia overview

A
AR - Sulfate transporter gene
Rigid clubfeet - need release in 50%
Cervical kyphosis
Scoliosis
Hitchikers thumb and califlower ears
221
Q

Diseases associated with Type II collagen mutations?

A

SED congenita
SED Tarda - late onset can be x-linked or AD
Kniest Dysplasia - AD, COL2A1
Stickler syndrome - AD, eye stuff,

222
Q

Sites of compression of the radial nerve?

A

FREAS
Fibrous bands (anterior to radial head)
Recurrent radial vessels (leash of henry) - cross PIN to supply mobile wad
ECRB
Arcade of Frohse (fibrous proximal supinator, most common)
Supinator (distal)

223
Q

Medial knee anatomy (layers)

A

Layer 1: Sartorius and fascia
- gracilis, semiT and saphenous nerve

Layer 2: Semimem, superficial MCL, MPFL, POL

Layer 3: Deep MCL, capsule, coronary ligaments

224
Q

Where does MCL and MPFL originate on the femur in relation to the ME, AT, GT

A

MCL is proximal and posterior to the medial epicondyle

MPFL is Anterior to the GT and anterior and distal to the AT.

225
Q

Lateral knee structures (layers)

A

Layer 1: ITB, Biceps femoris

Common peroneal nerve

Layer 2: Patellar retinaculum

Layer 3
Superficial - LCL, fabellofibular ligament, ALL
- Lateral geniculate between superficial and deep

Deep - Acruate ligament, coronary ligament, popliteus tendon, popfib ligament, capsule

226
Q

Types of meniscus tears?

A
Radial 
Oblique
Flap or parrot beak
Vertical/longitudinal
Bucket handle
Complex/degen
227
Q

Pediatric both bones treatment guidelines?

A

Plastic deformation - reduce if greater than 20 degrees angulation, 4 yo

Under 8 yo - 15-20 acceptable

Over 10 yo - 10 deg midshaft, 15 deg at distal 1/3
- Bayonet opposition acceptable in children under 10 years of age with 1cm shortening.

10 degree residual angulation = 20 deg loss of rotation.

228
Q

Study used to calculate incidence?

A

Prospective cohort study

229
Q

Bias vs. confounding?

A

Bias - systematic errors in methodology

Confounding - unaccounted variables that can explain associations

230
Q

How to examine bias in results of a meta-analysis?

A

Funnel plot

231
Q

Incidence vs. prevalence?

A

Incidence (inflow) - new cases per time period. Eg 10 per 1000 per year

Prevalence (Pool) - proportion of existing cases within a population

232
Q

Relative risk vs. odds ratio?

A

RR - ratio of incidence between two groups

OR - ratio of probabilities of an outcome between two groups

233
Q

How to interpret RR and OR?

A

RR - risk in exposed/risk in unexposed.

RR > 1 means risk greater than if not exposed. Use a 95% confidence interval that cannot cross 1.

234
Q

How is duchenne’s MD transmitted?

A

XR

235
Q

GMFCS levels predict what?

A

Long term motor function

Associated with increased rate of hip dislocation

236
Q

Prognosis for young children with CP to walk?

A

Ability to sit independently by age 2.

237
Q

Common type of test answer when looking to operate in CP question?

A

Spastic diplegia

238
Q

What releases will worsen gait in CP

A

Achilles in crouch gait - dont do alone with hamstring contractures

Hamstrings are overlengthened possibe to get stiff knee or anterior pelvic tilt.

239
Q

Common muscle transfers in CP?

A

Split Tib ant - dynamic supination in swing

Split tib posterior - hindfoot varus in stance

Rectus femoris for stiff knee (esp if stiff in swing)

Complete transfer of TA and TP are not recommended.

240
Q

Mechanism of botulinum toxin?

A

irreversible pre-synaptic block of release of Ach

241
Q

Indications for dorsal rhizotomy?

A

Ambulatory spastic diplegia (GMFC 1/2)

242
Q

Gene correlated with severity of disease in SMA?

A

Survival motor neuron II

SMA1 is the gene for SMN

243
Q

Blood volume for children?

A

75 mL/kg

244
Q

Diagnosis of compartment syndrome in children

A

3As

Anxiety, aggitation, increasing pain requirements

245
Q

AVN after pediatric femoral neck fracture

A
Increases with displacement and decreases with delbet type
I: 50-95%
II: 25-50%
III: 15-30%
IV: 5-15%
246
Q

Only strong recommendation from AAOS regarding femur fracture?

A

Children < 36 months be evaluated for child abuse

247
Q

In tibial spine fractures what is most commonly entrapped in the fracture site?

A

Anterior horn of the medial meniscus.

248
Q

Tolerances in pediatric tibial shaft fractures?

A

<1cm shortening, 5-10 deg angulation, 5 deg rotation

Risk of varus with intact fibula

Closed reduction, cast and weight bearing as tolerated.

249
Q

Age and reason you see transitional ankle fractures?

A

12-15

Distal tibia growth plate closes central - posterior - medial - lateral

250
Q

Surgical indications for pediatric distal tibia fractures

A

> 10 degrees of angulation (SHI/II) or >2mm intra-articular displacement

  • 50% growth arrest and greatest with medial mal (SH IV)
251
Q

Pediatric NAT - most common fracture locations?

A

Humerus, tibia, femur

Skin lesions most common lesion

252
Q

Diagnosis of child abuse?

A

40% sustain repeat abuse 5% death

Femur in non ambulator
Posterior rib fracture
distal humeral physeal
Metaphyseeal corner
Multiple fractures in different stages of healing
Patient age < 1 yo
253
Q

Syndromes associated with syndactyly?

A

Polands - syndactyly, absent sternal pec major, hypoplasia

Aperts - FGFR2 - acrocephalosyndactyly

254
Q

Most common type of pre-axial poly dactyly?

A

Type IV - duplicated proximal phalanx

Type II is number 2 - duplicated distal phalanx

255
Q

Post axial polydactyly

A

AD inheritance
AA > caucasions
If caucasian - genetic evaluation is recommended

256
Q

Types of Failure of differentiation?

A

Radioulnar synostosis
Syndactyly - simple vs complex (bone involvement) - 3rd webspace most common
Symphalangism
Camptodactyly - contracture (5th digit most common)
Clinodactyly - angulation in the radioulnar plane
Delta phalanx - physis not perpendicular to the long axis - excise bracket.

257
Q

Treatment of pre-axial polydactyly?

A

Associated anomalies are rare

Preserve bifurcated EPL/FPL and thenars

Collateral ligament reconstruction (radial collateral ligament)

258
Q

Acceptable pediatric proximal humerus fracture parameters

A

<5: 100% displacement, 70 deg angulation
5-12: 50-100% displacement, 40-70 deg angulation
>12yo: <50% displacement, <40 deg angulation

Closed reduction: 90 abd, 90 ER

Open fx = open reduction
Interposed - biceps, periosteum, muscle gets open reduction

259
Q

Pediatric lateral condyle fracture parameters and complication

A

<2mm - cast/observe
2-4mm, hinged - CRPP +/- arthrogram
>2mm, malrotated - ORIF

Make sure to get an internal oblique XR

Complications - cubitus valgus, tardy ulnar nerve palsy, lateral spur (periosteal displacement)

Lateral approach must preserve posterior blood supply

260
Q

Treatment of radial neck fracture in peds?

A

Rule of 3s - <30 angulation, <3mm translation, 1/3 of radial head

If > 60 deg angulation try percutaneous reduction

261
Q

Pediatric forearm fractures - acceptable parameters?

A

< 8yo: 20 midshaft angulation, bayonet apposition, no rotation

> 8yo: 10 midshaft angulation, no rotation

Plastic Deformation
<4 yo: angulation <20 deg will remodel
>4yo: reduce anything greater than 20 deg.

262
Q

Cause of dorsal bunion in pediatric clubfoot?

Tx?

A

Dorsiflexed first MT and plantar flexed great toe

  • Weak achilles and PL from lengthening or release

Overpowered by strong FHL and TA

Tx: MTP plantar release, FHL transfer to MT neck, +/- plantar flexion osteotomy at bast of 1st MT.

263
Q

Deformity and XR of congenital vertical talus?

A

Ankle equinus with midfoot dorsiflexion, hindfoot eversion and forefoot abduction

Dorsal dislocation of navicular on talus

50% due to genetic or NM causes.

XR - lateral view in plantar flexion - axis of 1stMT above talus (navicular does not ossify until 3 years, infer position with 1st met) - rules out oblique talus which reduces with plantar flexion

Lateral view in dorsiflexion - no correction of vertical talus

264
Q

What condition do you need to rule out with metatarsus adductus?

A

Skew foot - adducted forefoot with hindfoot valgus and lateral navicular subluxation with a plantarflexed talus.

265
Q

Benign pediatric foot conditions

A

1) Metatarsus adductus - 85% resolve
Calcaneovalgus foot - extreme dorsiflexion - A/w PM tibial bowing, L5 spina bifida, observe and stretch

2) Flexible flatfoot - normal until age 5, if asymptomatic in adolescents observe, stretching/arch support if painful. RARE for surgery - calcaneal neck lengthening or 3C osteotomy.
3) Osteochondroses - Severs (calcaneal apophysitis), Iselin disease (5th metatarsal apophysitis).
4) Kohlers disease - navicular AVN - SLC can decrease symptom duration, no bx, no MRI.

266
Q

Pediatric osteotomies

A

Redirectional

1) Salter - single innominate
2) Steele - Tripple innominate
3) Ganz - Periacetabular

Recontouring - hinge on triradiate

1) Dega
2) Pemberton
3) San Diego

Salvage - rely on fibrous metaplasia

  • Chiari
  • Shelf
267
Q

3 main types of rickets

A

1) Familial hypophosphatemic (vitamin D resistant) - due to impaired renal tubular phosphate absorption - XLD (PHEX gene). Treat with vit D and phosphate
2) Hypophosphatasia - AR due to defect in alkaline phophatase - Low alk phos and high urine phosphoethanolamine
3) Nutritional - genu varum treat with vitamin D

268
Q

Pediatric conditions associated with C1-2 instability?

A

Mucopolysaccharidoses (including Morquio)
Pseudoachondroplasia
SED
Down syndrome

269
Q

Injury Severity Score calculation?

A

Sum of square of 3 highest AIS scores (head/neck, face, thorax, abdomen, pelvis, extremities.

  • Any score of 5 = 75
  • ISS > 15 frequently used as definition of major trauma.
  • Correlates with mortality, morbidity, length of stay
  • Does not take into account bilateral injuries
270
Q

How much blood can be lost before drop in BP?

A

30% (around 1500 cc)

Class 1 - 15%
Class 2 - 15-30%
Class 3 - 30-40%
Class 4 - >40%

271
Q

Humeral shaft non-operative indications?

A

AP angulation < 20 deg
Varus/Valgus < 30 deg
< 3cm shortening

  • Very distal shaft fractures may have acceptable results with bracing if low demand.
272
Q

Imaging to see column of bone between AIIS and PSIS for supra acetabular pins?

A

Obturator outlet oblique

273
Q

Acetabulum classification

A

Elementary
- PW, AW, PC, AC, Transverse

Associated
- T shaped, Transverse with PW, Posterior Column/Wall, ACPHT, ABC.

274
Q

Tibial shaft non-operative parameters?

A

<2cm shortening
50% cortical apposition
Varus/valgus <5 deg
Flex/Ex < 10 deg

Intact fibula fisk for varus mal-alignment

275
Q

BMPs used in tibia

A

BMP2 approved as adjuvant for open tibia

BMP7 for non-union

276
Q

RUST Score

A

Tibial shaft fractures - breaks up into 4 areas (anterior, posterior, Medial, lateral)

Score per cortex (1-4)

1: absent callus, visible fx line
2: Callus present, visible fx line
3: Bridging callus, visible fx line
4: Remodeled cortex, invisible fx line (modified)

Standard 10 or modified 14 provide evidence of union.

277
Q

FDA definition of non-union

A

No progression of healing on 3 sequential monthly x-rays

NO progression of healing over 4-6 months.

278
Q

Most common intercarpal coalition?

A

Lunotriquetral

279
Q

Intercarpal wrist ligaments

A

SL - Dorsal strongest, tear leads to DISI and SLAC

LT - Volar stronger, leades to VISI

280
Q

Thumb CMC joint ligaments?

A

Primary is the Volar beak ligament

Dorsalradial ligament is second most important.

281
Q

Vascular supply to the hand?

A

Radial and ulnar arteries - Ulnar dominant in 88%

Superficial arch from Ulnar and deep arch from radial artery.

282
Q

Blood supply to the scaphoid?

A

Volar carpal branch and dorsal scaphoid branch both from the radial artery.

Volar carpal branch is the primary supply.

283
Q

All sensory axons have cell bodies where?

A

Dorsal root ganglion

284
Q

Intervals where median, ulnar, and radial nerves enter the forearm?

A

Median - Superficial and deep head of the pronator teres

Ulnar - superficial and deep head of the FCU

Radial - superficial and deep head of the supinator, found between brachialis and BR.

285
Q

Nerve interconnections in the forearm?

A

Martin-Gruber 10-25%

Richie-Cannieu <10%

Both median to ulnar

Both motor

286
Q

Anatomy of the lumbrical muscles?

A

4 total

From FDP tendon

Join interossei radially to form lateral band

Attach on dorsum of middle phalanx, distal phalanx

Flex MP, extend PIP/DIP

287
Q

Anatomy of intrinsics?

A
Interossei 
PADS (palmar, adduction) - 3 (long finger cannot adduct)
DAB (dorsal, abduct) - 4

From metacarpals join lumbricals to form lateral band.

Attach on dorsum middle phalanx, distal phalanx

Flex MP, extend DIP/PIP - all ulnar nerve

288
Q

Thenar Muscles

A
Abductor pollicis brevis
Opponens Pollicis
Flexor Pollicis Brevis - superficial and deep heads
- Thenar space palmar to Adductor
Adductor pollicis

APB is most important for Abduction/opposition

APB, OP, Superficial head of FPB - medial nerve

Deep head FPB and Adductor - Ulnar nerve

289
Q

Hypothenar muscles

A

Palmaris Brevis
Abductor DM
Flexor digiti minimi brevis
Opponens digiti minimi

All innervated by the ulnar nerve.

290
Q

Most common anomalus intrinsic extensors?

A

Extensor digitorum brevis from dorsal radial carpal ligament

Can present as a mass on the dorsum of the hand.

291
Q

Leddy classification?

A

Zone 1 flexor tendon injuries

1: to the palm must be fixed within 9 days
2: Retracts to A2 - 3 months - retraction prevented by vinculum longus
3: Retracts to A4 - retraction prevented by bone fragment - most common

292
Q

Zone III extensor tendon injuries?

A

INjuries to the central slip

Loss of active extension and flexion posture

Closed treat closed - splint for 6 weeks, open treat with repair and I&D

Untreated injuries lead to a buotonniere deformity

293
Q

Best prognosis for extensor tendon injuries?

A

Zone VI (Over MCPs)

294
Q

Quadrigga vs. Lumbrical plus finger

A

Quadriga - inability to make full fist from incomplete excursion of noninvolved tendons

Lumbrical plus - extension during attempted flexion - treat with release of radial lateral band (lumbrical).

295
Q

Dequervains tenosynovitis tendon involvement

A

First dorsal compartment - APL can have several slips and EPB can be in its own tendon sheath.

EPB is more dorsal

Injection works 50-80%

296
Q

Intersection syndrome

A

ECRL/B as they intersect over APL/EPB

297
Q

Tendon transfer for radial nerve palsy

A

PT to ECRB (not ECRL)

FCU to EDC (2-5)

PL to EPL

298
Q

Most common congenital hand anomaly?

A

Syndactyly - 1:2000 live births

Complete, incomplete, simple, complex

Most common between long and ring fingers.

299
Q

Most common polydactyly?

A

Post-axial - AD inheritance

300
Q

Digit anomalies?

A

Camptodactyly - flexion deformity

Clinodactyly - lateral deviation

Kirners derofmity - volar curvature of distal phalanx

Symphalangism - failure of finger IP joint development

301
Q

Blood supply to the thumb?

A

Princeps pollicis

Arises directly from the radial artery or the deep palmar arch

302
Q

Kienbocks disease classification and treatment

A
Lichtman
Restorative procedures
I: Norm XR, MRI positive with diffuse low T1 signal
II - XR with sclerosis, no collapse
IIIa: lunate collapse, normal alignment

Salvage procedures
IIIb: lunate collapse, DISI
IV: Carpal DJD

Restorative: Joint leveling (Radial shortening if ulnar negative or capitate shortening if ulnar positive), revasc, radial metaphyseal decompression

Salvage: partial fusion, PRC

303
Q

Muscles most affected in forearm compartment syndrome?

A

Deep - FPL, FDP, PQ

304
Q

Most common cancer of hand and most common sarcoma of hand?

A

Cancer: Squamous cell

Sarcoma: Epitheloid sarcoma

305
Q

Treatment indications for dupuytrens disease

A

MP joint contracture > 30 degrees

Any PIP joint contracture

306
Q

What is not affected in dupuytrens disease?

A

Clelands ligament

Transverse palmar ligament

307
Q

Spiral cord formed from what and does what to NV bundle?

A

Pretendinous band, spiral band, lateral digital sheet, graysons ligament

Brings NV bundle superficial, proximal, and midline

308
Q

Most important aspect for z-plasty?

A

All limbs of equal length

60deg increases length by 75%

309
Q

Cross finger flap vs. reverse cross finger flap

A

CFF: tissue from dorsum of a finger to palmar surface of an adjacent finger
- large palmar oblique

rCFF: palmar skin to cover dorsal wound

310
Q

Innervated local hand flaps?

A

VY - transverse or dorsal oblique finger tip amps, can preserve sensation in musicians

Moberg advancement: Thumb only can advance up to 1.5 cm

Neurovascular island flap: severe thumb pulp defects - usually ulnar side of ring or middle finger.
- Best axial flap for digital amputations

311
Q

Best hand flap for defects on the dorsum of the fingers, thumb?

A

Dorsal metacarpal artery flap - volar dorsal perforator found at the metacarpal head - raised on a proximal antegrade or reverse flow

If dorsal proximal phalanx - axial flag flap

312
Q

Common chemical burns and treatments?

A

Hydrofluoric acid (industrial cleaning) - Ca Gluconate

Elemental sodium (meth) - mineral oil not water because it will explode

White phosphorus (fireworks) - copper sulfate to identify particles and submerge in water

313
Q

Digit replant indications?

A
Thumb
Multiple fingers
Single finger distal to FDS
Hand, wrist, arm
Child

Order of repair - BEFANV
Bone, Extensor tendon, flexor tendon, artery, nerve, vein

If multiple digits do structure by structure

314
Q

What gives nerves tensile strength and elasticisy?

A

Epineurium

315
Q

Median nerve laceration commonly occurs with injury to what tendon?

A

FCR

316
Q

CRPS 1 vs 2

A

Type 2 has an identifiable nerve injury

317
Q

Strength/sensory return after carpal tunnel release?

A

Pinch strength by 6 weeks

Grip strength by 12 weeks

Continued weakness with sensory symptoms likely a transligamentous motor branch.

318
Q

Endoscopic vs open carpal tunnel?

A

Endo: lower post-op pain, higher risk of nerve injury, 44% more expensive

319
Q

Ligament vs. Arcade of struthers

A

Ligament: Median

Arcade: Ulnar (both start with vowels)

320
Q

Types of thumb CMC fracture?

A

Extra articular

Particular articular (Bennett) - stable piece connected to trapezium via anterior oblique ligament
Complete articular (Rolando)
321
Q

Deforming forces of base of thumb metacarpal fractures?

A

Adductor pollicis (adduction and supination) - ulnar nerve

APL (radial and proximal) - radial nerve (PIN)

322
Q

Healing of scaphoid fractures by pattern?

A

Distal pole > Waist > Proximal pole

Oblique > transverse

323
Q

Acute scaphoid fracture management?

A

Stable waist/distal pole - nondisplaced no diff in LAC, SAC, thumb spica (Doornberg JOT 2011 meta analysis)

Unstable waist - headless compression screw

Proximal pole - always surgery, high non union rate

Relative surgical indicaitons - smokers, delayed presentation

324
Q

Normal distal radius XR parameters?

A

11-22-11

11-12 mm radial height
22 deg radial inclination
11 deg palmar tilt

325
Q

Acceptable position for distal radius fractures?

A

< 10 deg dorsal angulation
Radial shortening < 3mm
<2mm joint step off

326
Q

SLAC Wrist arthritis pattern

A

Stage 1 - Styloid - excision, partial wrist fusion (STT, SC)

Stage 2 - Scaphoradius DJD - scaphoid excision and 4 corner fusion

Stage 3 - Proximal capitate migration, capitolunate DJD - 4 corner fusion or wrist fusion

Stage 4 - Pan carpal DJD - wrist fusion

327
Q

4 corner fusion entails what?

A

Scaphoid fusion and fusion between Lunate, capitate, hamate, and triquetrum.

328
Q

SLAC reconstruction options

A

4 corner fusion with scaphoid excision

PRC

With both 50% motion and 50% strength

329
Q

Tendon rupture treatments in RA

A

EPL rupture - tendon transfer with EIP or ECRL

FPL most common (Mannerfelt) - transfer with FDS to ring, BR or IP joint fusion)

330
Q

Late complication of isolated PCL?

A

Patellofemoral and medial chondrosis

331
Q

Where do most popliteal cysts occur?

A

Between the medial head of the gastroc and the semimembranosus

332
Q

What is miserable mal alignment syndrome?

A

Femoral anteversion, genu valgum, external tibial torsion