Stanford 1 Word Scramble
|
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Question | Answer |
name 2 braided and 2 monofil nonabsorb sutures | braided: silk, ethibond; monofil: prolene, nylon |
name 4 absorb sutures | chromic/plain gut, vicryl (braided), monocryl (monofil), PDS (monofil) |
name 2 categories of lvls of evidence | size of the effect (I-III), certainty/precision of tx effect (A-C) |
describe categories for size of effect for EBM | I: benefit >> risk, II: benefit>risk; III: risk> or = benefit |
describe categories for certainty/precision tx effect for EBM | A=mltpl RCTs or meta analysis (mltpl popul analyzed), B=1 RCT or mltpl nonRCTs, C=consensus opinion, case studies or std of care |
indications for sx for asympt AS and lvl of evidence (4) | Class IC: if severe AS w other sx or EF 50% or less; Class IIbC: severe AS w abnl response to exercise (can't incrsd SBP 20); Class IIaB: mod AS w other sx |
periop mortality AVR, incl if also CABG | 3-4% (STS database), 6% if also CABG |
risk factors for rapid progression in AS | >50yo, severe Ca++, CAD, |
avg change in severe AS velocity jet and AVA | change in velocity 0.3 m/s/yr, AVA 0.1 cm^2 |
describe Gorlin conundrum | formula for AVA doesn't calculate AVA well in low flow states |
better ways to assess AS in low flow states | AV resistance and stroke work loss |
likelihood severe asympt AS will be free of sympt 5y | 50% |
once sympt present in AS survival | angina 3 yrs, symcope 2y, CHF 1.5y |
term for pulse in AS | parvus et tardus |
Gorlin eqn | CO/(HR x ejxn time x 44.3 x mean gradient) |
describe Moore study on prosthetic pt mismatch in AVR | affects survival if <70yo (although Dartmouth grp showed difft results if use geomet dimensions) |
describe cutoffs for prosthetic pt mismatch | severe EOA/BSA <0.65, moderate 0.65-0.85 |
cut offs for AS jet velocity, mean gradient, AVA | jet velocity, gradient, AVA: mild= <3, <25, <1.5; severe= >4, >40, <1 |
what is the AVA index for severe AS | <0.6 |
MC BAV | Type I L-R (71% in Stanford study)--also assoc w coarct |
genetics assoc w BAV | eNOS thgt assoc, NOTCH involved in BAV and Ca++, ACTA2 SMaA famTAAA and dissections and BAV |
% coarct w BAV | 50-75% |
Sievers Ross v AVR study | used propensity matching and no diff survival and both same as general population--but Ross had more reoperations, no diff in thromboembol |
Yacoub Ross v homograft study | at 10yrs homograft did worse and transvalv gradient steadily incrsd; Ross did same as gen population |
what % severe AS don't undergo surgery | 30% |
pts enrolled in Ib part of Partner trial | severe AS AVA 0.8, grad 40, velocity 4, inoperable=10% STS risk score or predicted death 15% 30d; exclusion: >3 AR, BAV, no Ca++, EF <20%, CAD needing revasc |
results Ib Partner | 1 yr mortality 30.7% v 50.7%; 30d TAVI had higher stroke (5% v 1.1%) and vascular cxns (16.2 v 1.1%). 11% mod or severe paravalv regurg |
which valve used Partner | Sapien |
cut offs for MS (mean gradient, PA SP, valve area) | mean gradient, PA SP, valve area: mild <5, <30, >1,5; severe >10, >50, <1 |
what's nml MV area | 4-5 |
timeline of MS s/p RhF | 20-40y, once limiting sympt survival 0-15% 10y and once pul HTN mean survival 3yrs |
indication for sx in MS | Class IB NYHA III-IV mod or severe MS; CLassIC mod or severe MS + mod or severe MR; Class IIaC: severe MS + PASP >60, NYHA I-II |
how much does MA contract and timing | 20-40%, 89% occurs before LV cxn, which depends on strength and duration of atrial cxn |
describe MV leaflet open and closure | leaf open starts in ctr w edges still opposed, middle then commissures…leaf closure initiated by LA cxn |
cut offs for AR (angio grade, vena contracta width, regurg vol, regurg %, ERO) | (grade, VC width, regurg vol, regurg %, ERO): mild: 1+, <0.3, <30, <30, <0.1; severe= 3/4+, >0.6, 60, 50, 0.3 |
how does heart compensate for AR at sarcomere lvl | sarcomere added in series so nml preload at sarcomere lvl, but incrsd wall stress (incrsd chamber size), also incrsd afterload leads to hypertrophy…so both P and vol overload |
indications sx for AR | Class I: sympt, chronic severe; chronic severe asympt if EF<50 (Class I) or ES >50 (Class IIb); if moderate AR and sx on asc Ao or CABG (Class IIb) |
what's the name of bobbing head sign in AR | de Musset sign |
name of pulse in AR | Corrigans pulse or water hammer P (bounding pulse) |
name of murmur in AR | Austin Flint (1836-1915, president of AMA 1884) |
med tx for AR | afterload reduction w ACEI/nifedipine to reduce SBP, but don't use if no HTN |
describe what happens in IVC in AV fxn | just before AV opens Ao root expansion helps leaflets open, NC (connected to fibrous part MVAC) expands least, also longitudinal expansion of root |
describe what happens AV during ejxn | ann cxn (NC least), while commissures continue to expand (Lansac found base cont'd to expand), LC and NC clockwise torsion, RC CC. amt of torsion predict dP/dt while EF predicted ann cxn |
describe what happens AV during IVR | ann cxn asymm, commissures symm, longitudinal compression, when min LVP decrses work shifted to L base |
describe what happens AV during diastole | just recoil |
what's the diff dynamics and kinematics | kinematics is 3D location, by understanding dynamics (constitutive eqns) given boundary conditions can solve for kinematics |
types of MR by Carpentier classif | I=nml leaflet motion , annular dilation or endocarditis; II=prolapse, floppy MV w chord elong/rupture; III=restricted motion, A=diastole, B=systole, in rheum A+B, IMR=B, DCM=B + annular dilation |
% of CHF w FMR. % FMR s/p inferior MI | 40% of CHF and 40% inferior infarct (bc PM pap displaced laterally) |
causes of MR in W Countries | 70% degen w prolapse, 20% ischemic w tenting, 2-5% ea endocarditis and rheym |
cut off to consider MVP | 2mm above annulus |
cut offs MR (angio, VC width, MR vol, MR %, ERO) | (grade, VC width, regurg vol, regurg %, ERO): mild: 1+, <0.3, <30, <30, <0.2; severe= 3/4+, >0.7, 60, 50, 0.4…same as AR exc upper end of VC width and ERO |
indications sx for MR | ClassIB: acute severe sympt, chronic severe sympt NYHA II-IV EF>30% and/or ES >55, asympt chronic severe EF 30-60% and/or ES >40; ClassIIaB: asympt chronic severe EF>60%, ES <40 if repair >90% |
how much EF change s/p surgery | decrs 10% |
recurrence of MR after surgery | IMR annuloplasty (95% + CABG) in Cleveland incrs 3/4+ MR from 13 to 28% at 6mos…similar for difft ring types and smaller rings don't help |
LA and LV measurements that predict outcome | LA vol >40 means severe MR and predicts A fib; LVESVI >30ml/m^2 poor outcome |
how does MVP murmur change w loading | midsys click w late sys murmur, incrsd w standing and valsalva, decrs w squatting (same as HOCM and opposite of MR), handgrip incrses MVP murmur and decrses HOCM |
describe Crawford classif aneur | I=desc thoracic, II=desc and infrarenal **highest risk paraplegia, III=distal desc and infrarenal, IV=infrarenal |
describe deBakey classif | I=asc and desc, MC and worst px, II=asc, III=desc (b if also infrarenal) |
indication surgery TAAA | TAV asc 5.5, desc 6.5; MFS/BAV asc 5, desc 6; LDS: 4.5…4.5 if AV surgery, >1cm/yr grwth, dissection |
indications AAA surgery | 5.5cm or 2x nml, >0.5cm/6mo, any sympt |
types of endoleak | I=seal (prox or distal), II=bw branch vessel and sneur sac, ie IMA or intercostal, III=through graft, IV=incrs size aneur sac endotension |
preop mgmt of aneur/dissxn | MAP 60-80, HR 60, metoprolol, no SNP (decrsd afterload incrses shear and dP/dt)…decrsd SBP is to prevent rupture and anti impulse (decrs dP/dt) |
% dissxn w/o tear, how occurs | 13% no tear, thgt intramural hematoma from bleeding of vasa vasorum |
where dissxn tear in acute A | R anterior and sprials |
preop malperf acute A, how relates to mortality | Mohr 2009, if preop malperf 30% early mortality (v 14%), cor malperf and visceral worst; 48% cor resolve incl 60% paraplegia |
outcome for visceral malperf in acute A | 75% in hospital mortality |
overall mortality Acute A dissxn | 1-2%/hr, used to be 50% 48h, now if make 24hr, 10-20% 2d-5d, then 1%/d |
how many Acute A present w CP | 15-20% |
how many Acute A present w AI | 75% but in 85% can save native AV |
when take acute B dissxn to surgery | if rupture or intractable pain. Rupture actually did not incrs risk cxns or mortality |
op mortality Acute B Coselli | 22% and 6% paraplegia |
mgmt desc thoracic asympt and inoperable | no TEVAR, Demers Stanford study 2004, 5yr TEVAR 31% v 78% if operable (no comparison no tx v TEVAR) |
% aneur undiagnosed | 85% |
when is risk death highest s/p dissxn | first 2 yrs |
how many ppl get new aneury s/p dissxn | 20% get new aneur from dilation of residual false lumen |
who used cellophane to wrap aneur | Abott and Paulin in 1949 |
name for cystic medial degen | Erdheim dystic medial degen |
BAV and types of arches | I=Ao root (13%), II=incl tubular asc Ao (14%), III=tubular and trvrs (28%), IV=root, asc, trvrs (45%) |
should BAV Ao be replaced sooner | Class C, know BAV Ao abnl, grow more quickly, dissxn younger, but Yale study showed similar rate rupture, dissxn + better longterm survival (younger, healthier)…cxns not at smaller dia |
endovascular v med tx for uncomplicated B dissxn | INSTEAD trial showed no diff 2yr |
how much do Ao expand s/p TEVAR | 0.1cm/y asc, 0.3cm/yr desc and exacerbated by patent intercostals…tendency to dilate bc applies radial force |
what % dissxn have MFS | 5-9% |
% of MFS sporadic mutation, overall incidence MFS | up to 25%, overall incidence 1:5,000 |
who MFS named after, and when gene discovered | Antoine Marfan Fr pediatrician in 1896 who noticed in little girl, gene discovered 1991 |
systemic features MFS | arachnodactyly, high palate, jt hypermobility, flat feet, ectopia lentis, hernias, MVP, PTX, pectus, scoliosis |
role of fibrillin in eye | ciliary zonules |
key diff Loeys Dietz and MFS | hypertelorism, cleft palate/bifid uvula, aterial tortuosity, club feet, thin velvety skin w easy bruising, more diffuse medial degen |
mutation in LDS and how relates to TGFb signaling | TGFbR1,2 but increasd pSMAD2 suggests TGFb signalling is upregulated |
what rescues phenotype LDS in mice | losartan by blocking TGFb |
how freq famTAA in TAA, genetics | 19% TAA have 1st degree relative w TAA, present younger, assoc w TGFbR1,2; ACTA2, if also PDA assoc w MVHII |
what's arterial tortuosity syn? Genetics | AR glu transporter mutated (SLC2A10) and incrsd TGFb; they have facial dysmorphism |
mutation in Ehlers Danlos IV | vascular type of Ehlers Danlos, mutation Col III have pale translucent skin |
decsribe kyphoscoliosis type of Ehlers Danlos | type VI, due to lysyl hydroxylase mutation, fragile eyes and mscl wknss, very rare |
name 3 other syndromes w FBN mutations | 1) Shprintezene Goldberg (craniostenosis, MR; FBN1 and others); 2) Weille Marchesani (spherophakia round eyes, brachydactyly, stiff jt; FBN1); 3) Congen contractural arachno (crumpled ears, contractures; FBN2) |
describe features and genetics of homocystinuria | AR defect cystathionine synthase defic, Marfanoid w/o arachnodactyly, dwnwrd subluxation, hypercoag, MV/AV regurg w/o Ao dilation, MR, scoliosis, large stiff jts, often blond, blue eyed |
dx and tx homocystinuria | dx: decrsd methionine in urine and blood, tx B6 cofactor helps convert homocysteine to cystathionine, diet restrict methionine, ASA |
Created by:
ehstephns
Popular Midwifery sets