Basic science Flashcards
What type of collagen for Epithelial basement membrane?
Dupuytren’s?
Nucleus polposus?
Articular cartilage?
basement membrane: Type 4
Dupuytren’s: Type 3
Nucleus polposus: Type 2
Articular cartilage: Type 2
How does calcitonin inhibit osteoclasts?
Estrogen?
TGF beta?
Calcitonin: Interacts DIRECTLY with osteoclasts via cell surface raptors***
estrogen: Decreases RANKL* –> thereby stimulates bone production and prevents resorption
Also inhibits activation of adenylyl cyclase*
TGF-beta: Increases OPG***
How does PTH increase action of osteoclast?
1,25 dihydroxy vit D?
PGE2?
PTH: activation of PTH receptor STIMULATES adenylyl cyclase –> more cAMP*
PTH also binds to cell surface receptors on osteoblast to stimulate RANKL production*
1, 25 dihydroxy vitamin D –> stimulates RNKL expression
PGE2: activates adnylyl cyclase
Cell that osteoblasts are derived from?
How make bone?
Osteoblast differentiation?
Osteoblasts from UNDIFFERENTIATE MESNCHYMAL CELLS**
Make bone by producing non-mineralized matrix:
Alk phosphatase
Type I collagen
Osteonectin
Osteocalcin*** –> stimulated by 1,25 dihydroxyvitamin D
Differentiation:
BMP stimulates mesenchymal cells to become osteoprogenitor cells
Core binding factor alpha-1/RUNX2**
Stable beta-catenin plays a major role in inducing cells to form osteoblasts w/ resulting intramembranous bone formation**
PGDF induces osteoblast differentiation
IDGF induces osteoblast differentiation
How does PTH act on osteoblasts to make more osteoclasts?
PTH induces Jagged1 on osteoblasts***
Jagged 1 stimulates Notch receptors on membrane of hematopoietic stem cells –> cell proliferation –> more osteoclasts***
What cell line do osteoclasts come from?
Myeloid hematopoietic cells** –> from MONOCYTE/MACROPHAGE cell line*
Monocyte progenitors fuse tighter to form mature multinuclear osteoclasts***
How do osteoclasts resorb bone?
1: Howship’s lacunae –> sites of bone respiration where ruffled border meets bone surface **
2: Tartrate resistant acid phosphate –> secreted by osteoclasts to lower pH (using carbonic anhydrase) –> increases solubility of hydroxyapatite crystals
3: proteolytic digestion: organic material then removed by CATHEPSIN K (one of major proteolytic enzymes that digest organic matrix at ruffled border)**
How does osteoclast attach to bone?
Attaches at sealing zone***
Via INTEGRINS on osteoclast surface***
alpha-V-beta3 on osteoclast* is receptor for VITRONECTIN on bone surface**
Arg-Gly-Asp (RGD)* sequence of extracellular bone protein –> allows binding to integral on ostoeclast (Ab to to intern or RGD inhibit bone resorption)*
Which osteoprogenitor cells will become:
Osteoblasts?
Cartilage?
Fibrous tissue?
Osteoblasts: Low strain, high O2***
Cartilage: intermediate strain, low O2***
Fibrous: High strain**
What are main stimulators for osteoclast to resorb bone?
RANK-L***
IL-1***
Mesenchymal stem cell will differentiate into which of the following if exposed to:
PPAR-gamma?
MyoD?
Sox9?
C/EBPa
Runx2?
PPAR-gamma: Adipocyte***
MyoD: myoblasts***
Sox9: chondroblasts***
C/EBPa: adipocytes***
Runx2: osteoblasts***
Intermittent PTH tx targets which cells?
Osteoblasts* to form bone
PTH made by parathyroid glands (Chief cells)*** as 115 AA chain that is cleaved to 84 AA’s
Recomb PTH = 1-24 AA sequence at N-terminus***
What protein is most specific for mature osteoblasts but not expressed by immature proliferating osteoblasts?
Osteocalcin***
What is effect of 1, 25 dihydroxy vitamin D3 (active form)
Enzymatic conversion from 25 hydroxy vitamin D3 to 1, 25 dihydroxy vitamin D in kidney***
1,25 –> Increases resportion of Calcium in kidney to increase serum Calcium
Increases excretion of PO4- from kidney (decreases serum phosphate)***
Where is calcitonin made?
Calcitonin made in clear cells in the parafollicles of thyroid gland (C cells)***
Which part of bone is most responsible for compressive strength?
Proteoglycans* and Calcium hydroxyapatite*
type I collagen = TENSILE strength***
Blood supply to bone
What supplies inner 2/3 of mature bone?
Outer 1/3?
Growth plate?
Inner 2/3: arterioles from nutrient artery via aversion system***
Outer 1/3: Periosteal arterioles
Major source to growth plate: Perichondrial artery***
When does limb bud begin to grow?
How does it enlarge?
When can first be noted on transvaginal u/s?
Begins to form at 4 wks***
Enlarges due to interaction between the APICAL ECTODERMAL RIDGE and the MESODERMAL CELLS in the PROGRESS ZONE***
First seen at 8 wks***
What gene helps regulate first steps of limb development?
Notochord expresses Shh*** –> regulates limb bud formation
Limb patterning
Proximodistal?
Radioulnar limb growth?
Timing of radioulnar?
Proximodistal: First signal center to appear is APICAL ECTODERMAL RIDGE –> proximal to distal growth –> defect in AER = proximal limb truncation
FGF’s are needed in AER –> FGF8 is OBLIGATORY for normal limb development
Radioulnar: Second signaling center to appear is ZONE OF POLARIZING ACTIVITY along ulnar/posterior side
Grafting ZPA on anterior/radial side –> mirror image digit duplication***
Shh is dose dependent
High concentration on posterior/ulnar side to have small finger develop*
Low concentration on anterior/radial side for thumb to develop*
Abnormal UPREGULATION of Shh in ZPA = POLYDACTYLY on ULNAR side***
Downregulation = loss of ulnar digits
UPREGULATION on RADIAL side = loss of thumb***
Ulnar side formed earlier than radial side, so disruption of AP patterning will cause loss of later formed elements –> radius/thumb***
Dorsoventral axis embyrology?
Third signaling center (after AER and ZPA) –> non-AER limb ectoderm/WNT signaling center –> Progress zone**
Wnt = dorsal-ventral growth
Hox genes?
A/P or radioulnar patterning along with Shh***
Regulate somatization of the axial skeleton –> digit formation***
What is nucleus polposus from (embryology)?
Annulus fibrosus?
NP: notochord***
Annulus: Sclerotome***
During endochondral ossification at growth plate, what causes the most longitudinal growth of bones?
Chondrocyte HYPERTROPHY***
Not proliferation of chondrocytes***
What would deactivating mutation for PTHrP receptor do to growth plate?
Accelerate maturation in the zone of hypertrophy***
What is groove of Ranvier responsible for?
Perichondral ring?
Appositional bone growth***
Perichondral ring: dense fibrous ring that is critical for overall stability of growth plate***
Which region of physis does collagen type X play a role?
Zone of hypertrophy***
What does sclerostin do?
Sclerostin INHIBITS osteoblasts to DECREASE BONE FORMATION***
Work by binding the Wnt molecule***
How does phosphate administration decrease urinary calcium excretion?
Creates complex w/ calcium in the intestine to decrease available calcium for absorption***
Which BMPs exhibit osteoinductive activity? Which does not?
Which for ALIF?
Which for open tibial shaft?
Nonunion?
What BMP mutation leads to fibrodysplasia ossificans progressiva/stone man dz?
Osteoinductive: BMP 2, 4, 6, 7
BMP 3 = NO osteoinductive activity
BMP2* for ALIF (L2-S1, Medtronic cage), and for open tibia w/in 14 days of fx (IMN only, not plating*)
Nonunion of tibial shaft: BMP-7***
Mutation in BMP 4* = fibordysplasia ossificans progressiva*
How do BMPs work?
Activate mesenchymal cells to transform into osteoblasts –> produce bone***
Activate transmembrane SERINE/THREONINE kinase receptor**** –> SMADs*** (intracellular signaling mediators)
What is the most beneficial ultrasound signal for bone healing?
30mW/cm2 ***
Accelerates fx healing an increases mechanical strength of callus***
How do bone stimulators work:
Direct current?
AC current?
Pulsed EM fields?
Combined magnetic fields?
D/C: decrease osteoclast and increase osteoblast activity by REDUCING O2 tension and INCREASING pH***
A/C: Affect synthesis of cAMP***
Pulsed EM fields: causes CALCIFICATION OF FIBROCARTILAGE***
Combined magnetic fields: elevated concentrations of TGF-beta and BMP***
How does COX2 factor into bone healing?
Promotes fx healing by causing mesenchymal cells to differentiate into osteoblasts***
Fastest to slowest resorption rate for bone graft substitutes?
Calcium sulfate > tricalcxium phosphate > hydroxyapatite**
Osteoconductive vs osteoinductive vs osteogenic?
Osteocondcutive: material acts as STRUCTURAL FRAMEWORK –> DBM
Osteoinductive: Material contains factors that stimulate bone growth and INDCUTION OF STEM CELLS down a bone forming lineage –> BMPs
Osteogenic: Material directly provides cells that will produce bone –> mesenchymal stem cells, osteoblasts and osteocytes
DBM - osteoinductive vs osteoconductive?
BOTH osteoconductive and osteoinductive***
Contains collagen, BMPs***, TGF-beta, calcium
NO mesenchymal precursor cells
What synthetic has the highest compressive strength?
Calcium phosphate graft***
Tricalcxium phosphate, hydroxyapatite***
Shelf life for frozen or freeze dried grafts?
- 20 C: 2 years***
- 70 C: 5 years
Indefinite for freeze dried**
Chance of HIV, Hep C and hep B from fresh frozen allograft?
What are allografts checked for (diseases)?
HIV: 1 : 1,000,000
Hep C - 1 : 100,000
Hep B - 1 : 63,000
Allografts screen for***: HIV HBV HCV HTLV-1 Syphilis
What type of allograft substitute has more serous drainage?
Calcium sulfate***
What type of graft for ACL has the highest antigenicity?
Bone patellar tendon bone graft***
Due to the inclusion of bone***
Even higher than semimembranosus used to recon MCL (extra-articular)**
What to do if ACL graft grows bacteria if cultured during operation and has been implanted into patient?
Observation***
Rates 5-13% but none of studies showed that “contaminated” grafts developed clinical infection***
How often do bulk structural allografts fail due to insufficiency fracture?
Approximately 25% of time**
Anterior vs posterior iliac crest bone grafting?
Higher minor and major complications (significant) with anterior harvest***
Higher pain scores and duration of pain after anterior harvest***
What is lab test to look at vitamin D levels?
25-hydroxyvitamin D3**
What is the inactive form of vitamin D caused by high levels of the active form of vitamin D?
24, 25 dihydroxyvitamin D = inactive form formed in response to high levels of 1, 25 dihydroxyvitamin D***
Sarcomere composition
What happens with contraction to bands?
Thick myosin filaments***
Thin actin filaments***
Bands: H band/zone = myosin only*** I band = actin only*** A band = both actin and myosin*** Z line flanks each sarcomere and acts as site of attachment for actin filament***
During contraction:
A band - stays same length*
Both I band and H zone reduce in length*
What starts a nerve action potential?
Passage of sodium ions though voltage gated channels***
Ach is then released and diffused across synaptic cleft to bind to Ach receptor* (myasthenia pt has shortage of Ach receptors and botox blocks Ach release form end plate*)
Excitation contraction coupling:
In low Ca: tropomyosin blocks myosin binding sites on actin*
in HIGH Ca: Calcium binds to troponin on thin/actin –> configuration change of tropomyosin on actin* –> exposes myosin binding site***
Actin then forms cross bridge w/ myosin –> ATP breakdown –> two fibers contract past one another***
What are the two types of isotonic contraction?
Eccentric: muscle lengthens during contraction***
Concentric: muscle shortens during contraction***
Type I vs Type II muscle?
Type I –> SLOW TWITCH*** (slow red ox muscles)
Aerobic/oxidative phosphorylation
Exercise duration: endurance, low strength of contraction, low speed, FIRST TO ATROPHY with deconditioning
High yield ATP, requires O2 and thus are move VASCULAR
Increased mitochondria in cells
Type II - Fast twitch*
Anaerobic/glycotlytic
high strength/speed, fatigue rapidly (sprinting)
Low intramuscular TG stores*
Order of Recruitment:*
Type I fibers, then Type IIa (fast twitch, fatigue resistant) then Type IIb (fast twitch, easy fatigue)***
Metabolic systems for muscle energy
3 systems
1-ATP-CP anaerobic system**
Basis for creatine supplementation (main side effect = muscle cramping)
For intense metabolic exercise lasting LESS THAN 20 sec***
Coverts carbs stored w/in muscle
ANAEROBIC
2 - Lactic anaerobic system
Intense muscle activity 20-120 seconds (400 m)
Hydrolysis of one glucose molecule –> glucose to lactic acid + E
3 - Aerobic system
Use in longer duration and lower intensity exercises
Krebs cycle generates ATP from GLUCOSE and FATTY ACIDS through oxidative phosphorylation***
First cell to appear after acute muscle injury?
Neutrophil*** –> inflammatory cytokines –> swelling
Then macrophages that phagocytose debris
Then macrophages ass’d w/ muscle regeneration and scarring
Articular cartilage collagen type?
What molecule is responsible for hydrophilic behavior of articular cartilage?
Layers?
Type II collagen***
Aggrecan = responsible for hydrophilic behavior (proteoglycan)
Layers:
Superficial zone* –> type II collagen PARALLEL to joint, flattened chondrocytes, HIGHEST concentration of collagen, LOWEST proteoglycans**
ONLY ZONE where ARTICULAR CARTILAGE PROGENITOR CELLS FOUND*****
Intermediate zone
Random order to type II collagen, thickest layer
Deep/basal layer***
Type II collagen PERPENDICULAR to joint, HIGHEST PG, round chondrocytes in column
Tidemark
Divides superficial uncalcified cartilage from deeper calcified cartilage
Articular cartilage aging
Increases and decrease?
Advanced glycosylation end products?
Increases in:
Chondrocyte size*
Stiffness –> PASSIVE GLYCATION
Increased ratio of KERATIN SULFATE to chondroitan sulfate**
Decrease in: ABSOLUTE number of cells (hypo cellular) Water content***** elasticity proteoglycan size and number***
Advanced glycosylation end-products (AGEs)*
from spontaneous non-enzymatic glycation of proteins –> type II collagen cross linking –> increased stiffness/brittleness, increase susceptibility to fatigue failure
What does lubricin do?
Binds to HA to create a cross linked network***
Causes BONDARY lubrication***
Articular cartilage degeneration stages
First stage/early:
Water content INCREASES and PG aggregation and aggrecan DECREASE
More water = decreased stiffness –> more susceptible to damage
2nd/middle stage
Chondrocytes detect tissue damage and respond by releasing mediators to increase proliferation*** –> get clusters or cones of proliferating chondrocytes
3rd stage/late
Proliferative repose and anabolic activity are decreased –> get clinical signs of DJD***
What type of collagen increases with osteoarthritis?
Type X collagen***
Inflammatory response to allograft ACL vs autograft?
Inflammatory response is PROLONGED***
What does decorin do?
Most common proteoglycan in TENDON***
Regulates collagen fiber diameter –> length 300 nm, diameter 1.5 nm*****
How many vincula go to each FDS and FDP tendon?
2 vincula each* –> vincula longa and vincula brevis*
Just answer vincula brevis if asked on exam for which is torn (or both, but nearly never longa only)***
How does tendon enthesis sense nociception?
Free nerve endings in tendon enthesis***
In what phase after tendon repair is tenon weakest?
During inflammatory phase* (5-21 days*)
not cellular proliferation or remodeling phase
How do tendon fibroblasts detect applied strain?
Deflection of cell-cilia from tendon loading**
Types of cartilage:
Articular
Fibrocartilage
Elastic cartilage
Articular*
Articular surfaces, ribs, nasal septum
Water > collagen > PG > non collagenous protein > cells
Type II collagen*
Fibrocartilage*
Tendon/ligament, pubic symphysis, annulus fibrosis of disc, menisci*
Type I collagen* (95%, then some type III collagen etc)
healing response to microfracture*
Elastic cartilage***
Auricle of ear, epiglottis
Type II collagen with elastin
Which molecules have been linked to OA?
ADMTS-5***
Collagen type IX* (gene deletion in mice –> early OA in mice)*
Transcription vs translation?
Trasncription –> DNA to mRNA
Translation –> mRNA to protein
Cell cycle phases
G0 –> stable phase, DIPLOID cells (2N)
G1 –> initial growth has, DIPLOID (2N)
S –> DNA replication/synthesis phase, cells become TETRAPLOID (4N)
G2 –> Gap phase –> TETRAPLOID (4N)
M –> Mitosis phase
Southern vs Northern vs Western blotting?
Southern*
Restriction enzymes cut up DNA, separated on agarose gel –> get DNA sequence*
Northern*
mRNA cut up and separated on gel to identify RNA sequence*
Western*
Identifies PROTEIN*
What does reverse transcriptase PCR do? What then amplifies?
RT-PCR takes RNA –> DNA***
Then use regular PCR to amplify DNA (DNA –> DNA)***
What process is Tumor necrosis factor 1 involved with?
Apoptosis***
What cells can be antigen presenting cells/APCs?
B cells***
Dendritic cells***
APC breaks down protein antigen and presents via major histocompatibility complex receptors (MHC receptors) –> T cell receptor recognizes MHC/antigen complex to activate T-cell
Types of immunological reactions (Type I, Type II, II, IV)
Type I –> immediate anaphylactic*
Ass’d w/ allergy,, mediate by IgE activation of MAST CELLS and basophils*
Type II –> Ab dependent/cytotoxic hypersensitivity*** –> mediated by IgG and IgM
Type II: Immune complex (antigen bound to Ab) deposition type of hypersensitivity –> mediated by IgG and IgM Ab bound to antigen get deposited in diff tissues
Type IV* –> delayed type/cell mediated
Mediated by T cells, monocytes and macrophages**
Tb skin test**
Metallic implants**
What is Benign Ethnic Neutropenia and who has it?
Chronic inborn lifelong ANC below population mean –> NO INCREASED RISK OF INFECTION***
African descent and Middle Eastern patients***
Pedigree –> which are males and which are female?
Males = squares***
Female = circle***
Autosomal dominant vs recessive on which type of molecule they effect?
Autosomal dominant = defective STRUCTURAL PROTEINS ***
Autosomal recessive = defective ENZYMES***
Autosomal dominant Genetic pearls
Achondroplasia Apert CMT SED congenital MED type I MED type II Cleidocranial dysplasia OI (type I, IV)
Achondroplasia –> FGFR3
Apert - FGFR2
CMT - PMP22
SED congenital - COL2A1
MED type I: COMP
type II: Type IX collagen
Cleidoranial dysplasia: CBFA-1
OI type I, IV: COL1A1, COL1A2
Autosomal recessive Genetic pearls
Diasptophic dysplasia
Friderich’s ataxia
OI type II and II
Diastrophic dysplasia: DTD (sulfate transports protein)
Friedreich’s ataxia: Fratxin
OI type II, II: COL1A1, COL1A2
Translocation and gene product for:
Ewings?
Rhabdomyosarcoma?
Myxoid liposarcoma?
Synovial sarcoma?
Clear cells sarcoma?
Chondrosarcoma?
Ewing’s sarcoma: t (11:22), EWS-FLI1
Rhabdomyosarcoma: t (2:13), Pax3-FKHR
Myxoid liposarcoma: t (12:16), TLS-CHOP
Synovial sarcoma: t (X:18), SYT-SSX1, 2, or 4 fusion protein
Clear cell sarcoma: t (12:22), EWS-ATF1
Chondrosarcoma (Myxoid Variant), t (9:22), EWS-CHN
tumor antigens for:
Colorectal?
Pancreatic?
Ovarian?
Breast?
Hepatocellular?
Colorectal: CEA
Pancreatic: CA 19-9
Ovarian: CA-125
Breast: CA-15-3
Hepatocellular: AFP
What lab toll detects genetic translocations for prenatal screening?
Cytogenetic analysis***
Name 2 tumor suppressors
p53***
retinoblastoma gene Rb-1***
What does sensitivity test?
formula?
Probability that test results will be positive in pt with the dz***
sens: TP/ (TP + FN)**
a/ a+c
Specificity? formula?
Prob test will result negative in pt w/o dz***
spec: TN/ (TN + FP)***
b/ b +d
False positive? formula?
Pt w/o dz who test positive
b/ b+d
FP / FP + TN
1 - sens***
False neg? formula?
pt w/ dz who tests neg
c / a+c
FN / FN + TP
1 - spec***
PPV?
Prob pt w/ positive test has dz
Dependent on PREVALENCE of dz**
PPV = TP/ TP + FP PPV = a / a+b****
will give prevalence –> put in bottom columns, so if given prev 10% put 10 in bottom total column, and 90 in bottom right column, then use sens and specificity to fill out table, then use formula
disease pos disease neg test pos true positive a (9) false positive b (4.5) test neg false negative c (1) true negative d (85.5) TOTAL a+c (10) b+d (90)
NPV
NPV = d / c+d*** NPV = TN/ TN+ FN
prob neg test does not have dz
dependent on prevalence***
Likelihood ratio
Likelihood that given test result would be expected in pt with the large disorder compared to likelihood same result would be expected in patient WITHOUT target disorder
+ LR = sens / (1-spec)*
describes how likelihood of dz is changed by a positive test result*
- LR = spec / (1-sens)***
Incidence vs prevalence
Incidence: Number of NEWLY REPORTED cases of dz in specified time per unit measurement of population
Prev: TOTAL NUMBER cases at any time point
Relative risk
Risk of developing dz for people with KNOWN EXPOSURE compared to risk of developing dz without exposure –>used for COHORT SUTDY***
When RR > 1 incidence of outcome is greater in exposed/treated group***
[(a/a+b) / (c/c+d)]
Odds ratio
Odds that outcome will occur given particular exposure, compared to odds outcome will occur w/o exposure
Used for CASE-CONTROL (retrospective)**
OR = (a x d) / (b x c)
Number needed to tx
NNT = 1 / ARR***
Power (stats)
Estimate of probability a study will be able to detect a TRUE EFFECT of intervention
Power analysis performed PRIOR to starting study***
Power = 1 - (prob of type II error, beta error)**
Type II error = detecting NO difference when there IS A difference*
-AKA: accepting null when it should be rejected**
Type II error vs type I error
Type II error = detecting NO difference when there IS A difference*
-AKA: accepting null when it should be rejected**
Power = 1 - type II error***
Type I error = Rejecting null even though it is true*
AKA: Saying there is a difference when no true difference is present*
Type I error related principle: Bonferroni correction*
Post hoc stat correction made to P value when several dependent or independent stats tests are being performed simultaneously on single data set*
Confidence interval
Interval that will include a specific parameter of interest if experiment is repeated***
What test to use for normally distributed data means?
Non parametric/skewed mean?
Comparing proportions/CATEGORICAL data?
Comparing proportions in categorical data If low occurrences or small data set?
When comparing three or more groups?
Normally distributed mean: Student t test***
Non parametric/skewed set mean: Mann Whitney or Wilcox rank sum***
Comparing categorical proportions: Chi squared***
Low number: Fisher exact test***
3+ groups: ANOVA* (Kruskall Wallis if non parametric*)
What does funnel plot show?
Simple scatter plot of intervention effect estimates form individual studies
to detect PUBLICATION BIAS in meta analysis
ROC curve axis?shows?
Sens on y scale, 1- spec on x scale***
True pos on y scale = sens*
False positive on x scale = 1 - spec*
Used to determine RESPONSIVENESS***
Area under ROC = C statistic** –> used to compare different tests with higher C statistic better diagnostic
Area under ROC < 0.5 is useless test***
What is term for rejecting null when it is in fact true?
Type I error (alpha error)
Type I detect an effect that is not present***
What is Bayesian analysis?
Analysis starts w/ particular probability of event (prior probability) and incorporates new info to generate a revised probability**
RR is used in what type of study?
Cohort study***
ie: study on 500 pts undergoing THA followed and outcome assessed according to BMI***
Next of kin order?
Spouse Children (in no order) Parents Siblings Grandparents
How long on average before a physician interrupts a patient?
23 seconds***
Which is more favorable for surgeon, claims or occurrence coverage for malpractice?
Occurrence***
Provides coverage for all claims made during employment irrespective of when it was filed (during or post employment)
Claims: Only covers suits for the time employed***
What governing body determines if patient involved in workers comp claim can choose their treating physician?
State statute***
Most common successful malpractice against ortho?
Fasciotomies/ compartment syndrome***
How to decrease amount of radiation during case?
Place image intensifier (large round portion) as close as clinically possible to patient***
Image a smaller body part***
decrease time and amount of XR, use mini C arm, increase distance from C arm
How to define new patient for billing?
has not received services from physician OR any other provider in same practice group within past THREE YEARS***
Billing level determination
History, exa and medical decision making
Billing level is LIMITED TO LOWEST LEVEL of history, exam or medical decision making***
Modifiers for CPT codes
- 22 modifier: unusually complicated procedure
- 24 modifier: unrelated E&M (eval and management) during the postop period
- 25 modifier: significant or separate E&M performed on the day of procedure**
ICD 10 coding
First three digits?
Second three characters?
7th character?
First 3: category
4-6: anatomic site, laterality, severity, etiology
7th: Visit encounter sequela
Vancomycin time dependent or concentration dependent?
Time dependent*** vs tobra (dose dependent)
When do abx peak from cement, and how long do they stay bactericidal?
peak in 24 hours***
Stay bactericidal for 4 MONTHS***
What growth factor binds to and activates lipoprotein receptor related protein 5/6 (LRP5/6) during bone development?
Wnt protein***
Wnt binds to LRP5/6 at cell surface and activates intracellular cascade***
leads to translocation of beta catenin into nucleus –> activates transcription of genes that control osteoblast differentiation***
Highest sens and spec for PJI test?
Alpha defensin* (100% sens, 98% spec)*
Levels greater than 5.2 mg/L = 100% sens and spec for infection***
How does gabapentin work?
Reduces hyper excitability of VOLTAGE dependent PRESYNAPTIC CALCIUM channels***
How long to wait for elective surgery after DES placed?
6 months***
continue ASA through procedure***
Risk factors for not healing wound (lab values)
Zinc <95 mg/dL** (11.75 times risk of postop
lymphocyte count <1500
Ablumin <3.5 g/dL
Lovenox vs warfarin for VTE ppx?
Same efficacy to stop PE**
LWMW = HIGHER rate of major surgical site bleeding*
Lower rate of asymptomatic DVT*
how does Pazopanib work?
Anti-VEGF***
How much long acting insulin to take on day of ambulatory surgery?
Two thirds of usual dose***
NOT 1/2 (too often get hyerglycemic)***
