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PPT flashcards Surgical Biology

1
Q

What converts plasminogen to plasmin?

A

Tissue plasminogen activator (tPA)

Urokinase plasminogen activator (uPA)

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2
Q

Function of plasmin

A
  1. Clot dissolution – degrades fibrinogen & fibrin to FDPs
  2. Downregulation of coagulation – inactivates FVa & FVIIIa & degrades HMWK & prekallikrein
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3
Q

4 inhibitors of coagulation

A
  • Antithrombin
  • Heparin
  • Tissue factor pathway inhibitor (TFPI)
  • Protein C
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4
Q

Action of antithrombin

A

Anticoagulant – inhibits FVIIa, FIXa, FXa, FXIa, & FXIIa
Also decr inflamm
Heparin is cofactor

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5
Q

Action of heparin

A
  • Incr ability of antithrombin to interact w thrombin & thus incr activity of thrombin ~ 1000 fold
  • Also enhances release of TFPI which inhibits TF-VIIa complex
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6
Q

Action of protein C

A

Anticoagulant – inhibits FVa & FVIIa
Decr fibrinolysis – inhibits plasminogen activator inhibitor-1
Vit K dependent

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7
Q

Action of tissue factor pathway inhibitor (TFPI)?

A

Anticoagulant – inhibits FXa & TF-VIIa complex

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8
Q

3 inhibitors of fibrinolysis

A
  1. plasminogen activator inhibitor (PAI)
  2. alpha-2 antiplasmin
  3. thrombin activatable fibrinolysis inhibitor
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9
Q

Action of plasminogen activator inhibitor?

A

Inhibits plasminogen; incr inflamm

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10
Q

Action of thrombin activatable fibrinolysis inhibitor?

A

Antifibrinolytic – reduces conversion of plasminogen to plasmin
Incr inflammation
TAFI activated by thrombin, TAT complex, & plasmin (neg feedback)

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11
Q

Prothrombin time measures?

A

Extrinsic & common pathways

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12
Q

What does activated partial thromboplastin (APTT) time measure? What does activated clotting time (ACT) measure?

A

Both measure intrinsic & common pathways;

ACT is stall side test, less sensitive than APTT

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13
Q

Dx of DIC req primary dz + what clinicopathologic evidence of coagulopathy?

A

Decr platelets
Incr clotting times
Decr fibrinogen
Incr D-Dimers or FDPs

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14
Q

Treatment for DIC

A
  • Trt for endotoxemia
  • Transfusion of platelets/plasma (plasma contains AT which freq low in septic pts)
  • Heparin (incr activity of AT)
    LMWH greater inhibition of FXa; UFH assoc w prolonged APTT & decr PCV
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15
Q

Indications for whole blood transfusion

A

PCV < 20%
Blood loss > 30% blood vol
Oxygen extraction ratios > 40-50%
Incr lactate helpful

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16
Q

Calculation for how much blood to transfuse

A

25-50% total blood lost

Chronic blood loss:
L = [(PCVdesired-PCVpatient)]x 0.08BW(kg)/PCVdonor

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17
Q

How much RBCs lost into body cavity will be reabsorbed back into circulation?

A

Up to 75% w/in 24-72 hrs

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18
Q

Rate of adverse rxns to whole blood?

A

16% run, 2% fatal anaphylaxis

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19
Q

Topical hemostatic agents

A
  • Puffed gelatin sponge
  • Oxidized regenerated cellulose
  • Microfibrillar collagen hemostatic agents
  • Polysaccharide hemostatic agents
  • Bone wax
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20
Q

MOA of clenbuterol

A

Moderately selective B-2 adrenoreceptor agonist

Bronchodilator

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21
Q

Activated platelets in fibrin plug of wound direct & amplify early inflamm phase by release of?

A

PDGF & TGF-B

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22
Q

Processes that comprise proliferative phase of wound repair?

A
  • Angiogenesis
  • Fibrous/gran tissue formation
  • Collagen deposition
  • Epithelialization
  • Wound contraction
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23
Q

Angiogenesis in wound initiated by?

A

Decr O2 tension
Incr lactate
Decr pH in wound

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24
Q

Rate at which endothelial cells @ capillary tips grow in wounded area?

A

0.4-1 mm/day

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25
Q

Wound fibroblasts produce what type of collagen?

A

Type I collagen

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26
Q

Which factors regulate growth of capillaries in acute wounds?

A

VEGF

bFGF

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27
Q

What factors regulate fibroblast migration & proliferation?

A

PDGF
TGF-B
bFGF

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28
Q

Rate of re-epithelialization of equine wounds?

A

0.09 mm/day

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29
Q

How much can contraction reduce wound surface area by?

A

40-80%

58-76% reported for full thickness wounds in MC/MT area

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30
Q

Rates of wound contraction?

A

Wounds on body faster than distal limb

  1. 8-1 mm/day for body
  2. 2 mm/day for distal limb
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31
Q

3 reasons for wound contraction to cease?

A
  • Wound edges meet
  • Tension w/in surrounding skin equal/greater than that generated by myofibroblasts
  • When number of myofibroblasts in wound becomes low
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32
Q

What factors play a role in development of exuberant granulation tissue?

A
  • Prolonged inflamm phase (TGF-B1 & incr TIMP identified)
  • Microvascular occlusion
  • Bandaging
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33
Q

What is maintenance energy req for normally active nonworking horse?

A

33 kcal/kg/day

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34
Q

Protein req for adult horse?

A

0.5-1.5 protein/kg or

250-750 g/day

35
Q

5 ways airborne bacteria be controlled in OR?

A
  1. OR in low traffic location
  2. Maintain pos pressure in OR
  3. Filtering 90% of air
  4. 15 air exchanges per hour
  5. Air introduced @ ceiling & exhausted @ floor
36
Q

How long in sx before surgical gloves may culture pos?

A

15 mins

37
Q

Surgical gloves fail during what% of sx?

A

20%

38
Q

6 risk factors for SSI after GI sx?

A
  1. Sx time > 2 hrs
  2. Reoperation
  3. Inexperienced surgeon
  4. Near-far-far-near sutures
  5. Staples
  6. PG910
39
Q

4 protective factors for SSI after GI sx?

A
  1. Lavage of linea
  2. Topical abx @ closure
  3. In situ drape for recovery
  4. Minimize sx time
40
Q

Risk factors for SSI post-castration?

A
  • Lack of drainage
  • Lack of abx prophylaxis
  • Standing nonsutured technique
41
Q

Protective factors for SSI post castration?

A

Laparoscopic

Recumbent sutured technique

42
Q

% SSI after laryngoplasty and risk factors?

A

0-4%
Laryngotomy
Draft horse

43
Q

% SSI after arthroscopy and risk factors?

A

0.5-1.5%
Draft horse
Tibiotarsal joint

44
Q

MOA of metronidazole?

A

Disrupt bacterial DNA by free radicals & intermediate compounds

45
Q

MOA of tetracyclines?

A

Inhibits protein synthesis by binding reversibly to 30S ribosomal subunit

46
Q

MOA of macrolides?

A

Inhibits protein synthesis by binding reversibly to 50S ribosomal subunit

47
Q

Which antimicrobial classes are bacteriostatic?

A

Tetracyclines
Chloramphenicol
Macrolides

48
Q

Advantages & disadvantages of PMMA abx impregnated beads?

A

Adv easy to mix, abx last longer than plaster of paris

Disadv  not absorbable, heat labile abx cannot be used

49
Q

Adv & disadv of plaster of paris abx beads?

A

Adv inexpensive, absorbable

Disadv  abx leach @ rapid rate (~ 80% eluted w/in first 2 days), set up time slower than PMMA

50
Q

When are GFs secreted after PRP injection?

A

95% secreted within 1 hr

51
Q

What is optimal PRP concentration?

A

At least 3-5x baseline platelet count or @ least 1x106 platelets/ul

52
Q

Diffs btw adipose derived mesenchymal stem cells vs. bone marrow derived?

A
  • Adipose easier to obtain
  • Adipose yields more MSCs vs bone marrow (2% vs 0.002%)
  • Adipose have faster rates of proliferation
  • Adipose derived MSCs have greater immunosuppressive ability
  • Studies indicate little diff in regenerative & differentiation potential, growth kinetics, cell senescence, & efficiency of gene transduction
53
Q

What % of BM-MSCs form fibroblast colonies?

A

0.01-0.001%
Number decr w age
Quality of MSCs also decr w age

54
Q

3 effects assoc w UFH that are not assoc w LMWH?

A
  1. ↓ PCV
  2. ↓ platelet count
  3. Lower incidence of jug vein abnormalities with LMWH vs UFH (2003 study)
55
Q

According to Westerman et al. 2015 horses with increased ??? concentration @ 24-72 hours after admission were more likely to be euthanized or develop complications

A

Serum amyloid A

56
Q

According to Viljoen et al. 2014, tetrastarch @ 10, 20, & 40 ml/kg increased COP. Which dose was more likely to have changes in coat indicators?

A

40 ml/kg

57
Q

According to McKenzie et al. 2016, plasma and hetastarch comparably increased plasma COP for 48 hrs. What changes were assoc with Hetastarch vs plasma?

A
  1. Hetastarch & plasma comparably ↑ plasma COP for 48 hrs; max ↑ of 2.0 & 2.3 mmHg respectively
  2. Hetastarch infusion ↓ Hct, hemoglobin, TP, & albumin conc for 72-120 hrs
  3. Plasma infusion ↓ hemoglobin & Hct for 20-24 hrs, & ↑ TS for 48 hrs
  4. Platelet count & coag times minimally affected by plasma or Hetastarch
58
Q

What was the prevalence of antimicrobial assoc diarrhea according to Barr et al. 2013?

A

AAD prevalence 0.6% w 18.8% mortality rate in nonhospitalized horses treated for nonGI signs
Most freq used abx in horses w AAD were pen/gent, enrofloxacin, & doxycycline

59
Q

Incidence of nosocomial infection reported by Ruple-Czerniak et al. 2014?

A

19.7%

Most common - surg site inflamm & IV catheter inflamm

60
Q

Dose of gentamicin for neonates per Burton et al. 2013?

A
  1. Gentamicin @ 12 mg/kg q36h required in foals < 2 wks

2. Longer half life longer & volume of distribution higher in 1-3 d older foals vs. older foals

61
Q

Minocycline @ what dose achieved conc > MIC in blood, synovial fluid, & CSF according to Schnabel et al. 2012?

A

4 mg/kg PO q12h

62
Q

What was the incidence of catheter related complications in the study by Kelmer et al. 2012 in horses treated with IVRLP by indwelling catheters?

A

27%

  1. Indwelling cephalic or saphenous IV catheters for IVRLP in 44 horses w synovial injury of distal limb resulted in 87% resolution & 61% return to soundness
  2. Catheter-related complications in 27%; most (11/12) were phlebitis (5 saph & 6 ceph); no effect of catheter (6 polytetrafluoroethylene & 39 polyurethane)
  3. Horses w multiple synovial structures involved had more complications
  4. No complications occurred in horses w < 7 perfusions
  5. Horses w concurrent osteomyelitis less likely to have resolution of synovial infx
  6. RLP successfully used as ONLY mode of abx in 14 horses
63
Q

What was the conclusion of Zantingh et al. 2014 on the combination of amikacin & timentin for IVRLP?

A
  1. Use of amikacin w ticarcillin/clavulanate for IVRLP resulted in sig lower synovial fluid conc of amikacin & reduced antimicrobial activity in middle carpal joint @ 30 & 60 mins after tourniquet removal compared to amikacin alone
  2. Combination should be avoided
64
Q

According to Harvey et al. 2016 what was the effect of 3g amikacin vs 2 g on concentrations in the middle carpal joint vs fetlock joint?

A

Conc were higher in middle carpal with 3 g, but no diff in fetlock

  1. IVRLP w 3 g amikacin via cephalic vein w tourniquet for 20 mins resulted in higher amikacin conc in middle carpal joint @ 25 mins & 24 hrs vs 2 g amikacin; no diff noted btw doses for fetlock joint
  2. Target amikacin conc for S. aureus & coag-neg Staph achieved in both middle carpal & fetlock for both doses
  3. Target amikacin conc for E. coli & Actinobacillus sp achieved in middle carpal joint for 3 g dose
  4. Target amikacin conc not achieved for Enterococcus sp, Pseudomonas, or Strep zoo (this study used bacteria from their hospital, not previously published MIC number)
  5. Daily IVRLP recommended as PAE effect unlikely to last beyond 24 hrs
65
Q

What were the findings of Moser et al. 2016 when evaluating perfusate volume on amikacin conc in DIPJ & RCJ?

A
  1. IVRLP via cephalic vein w 1 g amikacin diluted in 10, 30, 60, & 120 ml volumes resulted in higher mean amikacin conc in DIPJ vs RCJ for all volumes
  2. Mean conc amikacin in DIPJ reached therapeutic levels for organisms susceptible & resistant to amikacin @ 10, 60, & 120 ml vols
  3. Mean conc amikacin in RCJ reached therapeutic levels for susceptible organisms for some vols, but was not therapeutic for resistant organisms for all vols
  4. All volumes resulted in immediate ↑ in mean regional intravascular pressure after perfusion
66
Q

What were the findings of Colbath et al. 2016 on the use of mepivacaine in IVRLP?

A
  1. Addition of mepivacaine to amikacin perfusate for IVRLP did not affect amikacin conc in synovial fluid of RCJ or in vitro antimicrobial properties of synovial fluid (zone of inhibition for S. aureus & E. coli)
  2. Mechanical nociceptive threshold was higher for amikacin + mepivacaine group vs amikacin only @ 30 mins after IVRLP before & after tourniquet removal
  3. Diff in MNT btw groups was abolished by use of sedation @ beginning of RLP & no measures were taken during RLP or after 30 mins
67
Q

Findings of Oreff et al. 2016 indicated that amikacin conc in fetlock was higher @ 30 mins with 2 g in 100 ml perfusate volume vs 30 or 60 mls. There was no difference in synovial fluid concentration how long after IVRLP?

A

2 hours

  1. Higher mean amikacin conc achieved in MCP joint @ 30 mins via IVRLP w 2g amikacin in 100 ml vol through cephalic vein compared to 30 & 60 ml vol
  2. More horses reached synovial therapeutic threshold following perfusion w 100 ml (100%) vs 60 ml (43%) or 30 ml (57%) @ 30 mins
  3. No diff in synovial fluid conc or critical therapeutic threshold @ 2 hrs – poss d/t body’s tendency to reach equilibrium poss supported by finding that serum amikacin conc sig higher @ 120 mins in 100 ml group
68
Q

What was the incidence and complications reported by Rubio-Martinex at al. 2012 after IVRLP & IORLP in horses?

A

Complications of IVRLP occurred in 12.26% - hematoma, phlebitis, thrombosis
Complications of IORLP were higher than IVRLP (33%) – screw loosening, screw breakage, difficult inj, & discharge around screw
Horses trted w established synovial infx had lower survival rate than horses w fresh minimally contaminated lacerations (+/- synovial involvement) – 53.4% vs 91.9%

69
Q

What was the effect of emptying the vasculature before IVRLP in Sole et al. 2016?

A

No diff in amikacin conc of RCJ

Incr amikacin conc of MCPJ

70
Q

Findings of Godfrey et al. regarding effect of perfusate volume on amikacin conc in MCP joints?

A
  1. Higher mean conc amikacin achieved in MCP joints of horses treated w 1 g amikacin via LPD vein in a 60 ml total vol vs 10 ml total vol
  2. Interstitial fluid samples obtained from the dorsolateral aspect of the midmetacarpus had greater amikacin conc @ 6 hrs for 60 ml perfusate vol vs 10 ml
  3. Peak venous BP in distal portion of limb significantly higher after 60 ml vs 10 ml vol; no diff in time to return to baseline
71
Q

Adams et al. 2013 found that which of 2 sequential 5 ml bone marrow aspirates from the ilium & sternum contained the highest cell counts?

A

The first 5 ml sample

72
Q

Kisiday et al. 2013 found that there was or was not a difference between drawing 5 mis or 50 mis bone marrow aspirate?

A

Found there was no benefit to drawing 50 mis over 5 mis

  1. Highest density of MSCs obtained from 1st of 2 sequential 5 ml fractions from ilium & sternum when 2x 5 ml & 2x 50 ml fractions drawn
  2. Overall MSC yield not significantly different btw 1st 5 ml & 50 ml fractions (no benefit of 50 ml over 5 ml)
  3. 2nd 50 ml fraction yielded few to no MSCs
  4. Chondrogenesis higher from ilium vs. sternum
73
Q

Findings of Whelchel et al. suggesting LMWH should be administered q12h?

A

Anti-factor Xa activity w/in or above thromboprophylactic range when admin q12h; fell below range ~ 16 hrs after admin when given q24h

There were no changes in PCV, platelet count, or AT activity

74
Q

What is a buffer?

A

Substance capable of donating or accepting a proton?

75
Q

What is ph?

A
  • log [H+]
76
Q

Where does gentamicin accumulate in kidney?

A

Renal tubular cells

77
Q

Why is prednisone not effective in horses?

A

Oral absorption is poor and hepatic metabolism to the active drug prednisolone does not appear to occur in horses

78
Q

Mechanism of action of steroids?

A

Inhibit AA cascade by blocking phospholipase A2

79
Q

Which steroids are 5x more potent than hydrocortisone?

A

Triamcinolone, methylprednisolone

80
Q

What are the similarities & differences of Atropine & Glycopyrrolate?

A

Anticholinergics = non-selective muscarinic receptor antagonists
 Parasympatholytic drugs = block PSNS effects
 Both increase heart rate, & decrease GI motility & oral secretions
 Atropine = M1, M2, M3
 Very selective for muscarinic, little effect on nicotinic receptors
 Sedative & ocular (mydriatic) effects
- produces drowsiness and potentiates effects of CNS depressant drugs because it crosses BBB
- crosses placenta
- duration of action: 60-90 mins
 Glycopyrrolate = synthetic quaternary ammonium
 No sedative or ocular effects
 4x as potent as atropine
 Absorption, metabolism, excretion like atropine-in urine
 Safer than atropine for treatment of intra-op bradycardia
o Does not cross placenta or BBB hence devoid of fetal or CNS effects
o duration of action 2-4 hours

81
Q

What is mechanism of action of Albuterol?

A

o B2 adrenergic agonist
o Inhibits tracheal smooth muscle contraction resulting in bronchodilation
o Decreases release of inflammatory mediators from mast cells
o Increase mucociliary clearance
o Side effects: sweating, muscle tremors, excitement
o REMEMBER that under GA bronchodilators have the effect of increasing anatomic dead space!!

82
Q

Mechanism of action of cisplatin & 5-FU?

A

Cisplatin - alkylating agent
5FU - antimetabolite: destroys tissue superficial layers (you can not control/ estimate depth), interfere with DNA and RNA synthesis by interaction with enzymes

83
Q

Mode of action of aminocaproic acid?

A

Derivative of the amino acid Lysine

Binds reversibly to plasminogen so that it cannot be activated

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