Digestive Flashcards

1
Q

Describe the splenic vasculature?

A

Celiac a.

  • hepatic
  • left gastric
  • splenic
    • pancreatic
    • left gastroepiploic
    • short gastic

Splenic v. ⇒ gastrosplenic v. ⇒ portal v.

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2
Q

What is the storage capacity of the spleen for rbc and platelets?

A

10-20% rbc mass

30% of platelet mass

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3
Q

What are the 3 major functions of the spleen?

A
  1. hematopoiesis: EMH fetal development, maturation of rbc, destruction of rbc, store iron (hemosiderin, ferritin). EMH dogs (uncommon cats)
  2. Reservior function: 3 pools - rapid (30 sec), intermidate (8min), slow (1hr)
  3. Immune: B-cells, T-cells, IgM, removal of IgG coated rbc/platelets.
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4
Q

What are the 4 mechanisms of generlized splenomegally?

A

inflammation, congestion, neoplasia/cell infiltration, cellular hyperplasia.

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5
Q

Difference between cat and dog spleen?

A

Dog: sinusoidal - combinaiton of direct arteriovenous AND areas where rbcs have transverse the red pulp before entering a sinus/venous side.

Cat: nonsinusoidal - open ended venous channels and perofrated endotheial channels = direct communication between arterial and venous vasculature.

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6
Q

Name causes of localized splenomegally - nine.

A
  1. Nodular hyperplasia: splenoma, fibrohistiocytic nodules (Cocker spaneils)
  2. Pseudotumor - benign lesion (plasma cells, histiocytes and lymphocytes)
  3. Hemangioma
  4. Haratoma - mature splenic tissue,, not normal structure
  5. Ascess - torsion, bacteremia, FB
  6. Cysts - humans
  7. Segemental infarction - poor profusion, hemobartenella
  8. Plaques - hemosiderosis, siderocalcific = hemosiderin, calcium, bilirubin
  9. Neoplasia: hemic vs. non-hemic
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7
Q

What are predisposing factors for splenic infarcts (9-10)?

A

Hypercoaguable = sx not recommended for seg. infarct due to risk

splenomegaly

cardiac, liver or renal disease

neoplasia

excessive corticosteroids

sepsis

splenic hematoma

vasculitis

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8
Q

On splenic US what is generally associated with the following:

Hypoechoic nodules

Diffuse hypoechogenicity

Hyperechoic nodules

Target lesions

multiple descreate lesions

A

Hypoechoic: lymphoid infiltration, infarction, necrosis

Diffuse hypoechoic: passive congestion, splenic torsion

Hyperechoic - nodular hyperplasia, neoplasia, fibrosis

Target lesions (hypoechoic rim): positive predicitve for malignacy

Multiple similar descreate lesion associated with maligancy

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9
Q

How does contrast enhanced (microbubble) US help define malignancy?

A

Malignant lesions have a different pattern than surrounding tissue. Accuracy similar to contrast MRI and CT

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10
Q

What changes are consistenty with malignancy on CT and MRI?

A

CT: lower Hounsfild units (pre and post contrast)

MRI: malignant hyperintense on T2 and postgadolinium

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11
Q

How does cytology compare to histopathology for splenic masses?

A

Variable but overall good for dx hematopoietic neoplasia and hyperplasia.

59% agreement, 29% partial agreement and 12% disagreement in one study

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12
Q

What stain can help ID cells of hmic origin?

A

Romanowsky

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13
Q

When dividing the spleen for a partial splenectomy, what are options?

A

TA stapler

2 clamps, cut inbetween and suture

CO2 laser

Ultrasonic cutting device

Biopolar electrosurigcal device

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14
Q

Ultrasongraphic appearence of splenic torsion?

A

Splenomegally, diffusely hypoechoic (also seen with necrosis and infarction)

6/7 dogs had hilar perivenous hyperechoic triangle

chronic may demonstrate gas shadowing

Absence of blood flow on color flow doppler US

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15
Q

What is the signalment for dogs with splenic torsion?

A

Large/giant deep chested dogs, MALES

Danes, St. Bernard, GSD, Irish setters

Poss. associated with spontaneous resolved GDV??

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16
Q

Percent of non-traumatic hemoabdomens with maligant cancer and what percent of these were HSA?

A

up to 80% malignant

of these 63-88% HSA

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17
Q

Percent of non-traumatic hemoabdomens with splenectomy that had arrythmias postop?

A

44%

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18
Q

What is the percent of arrhythmias associated with splenectomy for neoplasia and when are they more common?

A

35%

More common with anemia, hypotension, leukocytosis, and splenic mass rupture

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19
Q

What is it called when poor organ profusion occurs due to too tight of a closure of an abdominal hernia?

A

Abdominal compartment syndrome - associated with loss of domain.

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20
Q

What are the 4 priniciples of hernia repair?

A
  1. ensure viability of entrapped hernia contents
  2. release and return viable hernia contents into normal location
  3. remove reduntant hernia sac
  4. Provide tension free closure
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21
Q

Name 8 common sites for abdominal hernias

A

Paracostal, dorsal lateral, inguinal, femoral, perineal, cranial pubic ligament rutpure, umbilical, scrotal, ventral (subxyphoid)

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22
Q

How is the abdominal wall formed in embyro?

And what is the cause of an umbilical hernia?

A

Migration of the lateral, cephalic and caudal folds

Failure of the lateral folds to close

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23
Q

What passes through the umblicus?

A

umbilical blood vessels - (vein = faliciform lig)

Vitelline duct

stalk of the allantosis

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24
Q

What disease have been associated with umbilical hernias?

A

Fucosidosis = inherited neurovesical lysosomal storage disease

Ectodermal dysplasia

Cyrptorchidism

Other hernias and incomplete sternal fusion can co-exsist: ventral abdominal, diaphragmatic

Other midline defects and cardiac defects

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25
Q

What is gastroschisis and how is it different than an omphalcele?

A

It is a congential paramedian defect (omphalocele midline) exposing abominal contents.

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26
Q

What breed are at increased risk for umbilical hernia?

A

Airedale, basenji, Pekingese, pointers, weimerainers

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27
Q

Describe the boundries of the internal and external inguinal ring.

A

Internal: Medial rectus m., cr. internal abdominal oblique, lat/caudal: inguinal lig.

External: slit in apopneurosis of external abdominal oblique

Together form inguinal canal

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28
Q

What passes through the inguinal rings?

A

Gential branch of the gentifemoral a,v,n.

External pudendal vessels

Round lig (female), or spermatic cord

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29
Q

What is an inguinal heria that contains a gravid uterus?

A

Hysterocele

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30
Q

Three methods to repair a large inguinal hernia?

A

Own tissues

polyethylene mesh

cr. sartorius flap

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31
Q

Describe the femoral canal.

A

2 areas within the limits of the inguinal lig and pelvis.

  1. Muscular lacuna: Femoral n, and illiopsoas m.
  2. Vascular launa: femoral a, v, n and saphenous

Lacuna divided by the iliopectinal arch (iliac and transverse fascia = surrounds vasculature forming the femoral sheath)

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32
Q

What are risk factors for abdominal incision dehisence?

A

Increased intraabdominal pressure (pain), entrapped fat btwn edges of repair, inappropriate surture, infection, chronic steroid and poor postop care

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33
Q

What are methods to increase the strength of a prepubic tendon repair with mesh?

A

Mesh cuff with vertical mattress sutures

double layer mesh technique

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34
Q

What are factors associated with chronic incisional hernias

A

obesity, hypoproteinemia, cardiopulmonary complicaitons, absominal distension skin wound dehisence, and deep fasical infection

Local wound complcaitons most improtant

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35
Q

What are characteristerics of a desirable vascular muscle flap?

A

Avoid bulkiness

Avoid tension

Consistent vascular supply that is resistent to superfical trauma

Not result in significant loss of function

Be readily excessible

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36
Q

What are 3 major vascularized muscle flaps?

A

Cranial sartorius musle flap

External abdominal oblique myofascial flap

Latissimus dorsi

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37
Q

What is the origin and blood supply of the crainal sartorius flap?

What is it useful for?

A

iliac crest and lumbodorsal fascia

Branch of femoral a/v supplies proximal 1/3

Area covered: 30% caudal abdomen = transverse, 80% length btwn pubis and ribs

Used for prepubic, femoral and inguinal hernias

Delayed flap (distal blood supply) caudal abdominal repair in cats.

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38
Q

Describe the external abdominal oblique flap

A

Myofasical island flap (middle zone of the lateral abdominal wall)

Cr. branch of the cranial abdominal a. (hypogastric n and satellite v)

ventral, cranial to mid abdominal wall

10cm x 10cm area

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39
Q

Describe Marlex mesh.

A

Polypropylene mesh

inert

monofilament

woven

4-5mm fibrous tissue ingrowth by 6 months

Other meshes: Gore-tex (teflon) - permanent microporus, polygalctin 910 absorable

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40
Q

List biologic tissue grafts and their potential use?

A

SIS, dermis, pericardium

maybe useful for infected locations, avoids acute/chronic infection/inflammation

completely replaced with collagen in 4 months

Experimentally for abdominal wall defects, clinically for perneal hernias

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41
Q

What are three methods of mesh reconstruction? Which is better?

A

Onlay - more complications (_<_69% in people) increased infection, seroma, hematoma, extrusion = potentially due to more undermining/being superficial

Inlay - poor tissue interface

Underlay - best - lowest rate reherniation and wound complications = adhesions and enterocutaneous fisulas have been found in humans = need to use omentum

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42
Q

What are the surgical goals of abdominal herniorraphy?

A

Asepsis

tension free closure

use of strong tissue only

anatomaic closure

proper technical execution

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43
Q

What are the 4 major muscular and tendinous portions of the diaphram?

A
  1. central tendon: 21%
  2. Pars sternalis - xyphoid and 8th
  3. Pars lumbaris = left and right crus (R>L, lateral, intermediate and medial portions) - L3,L4 medial to psoas minor
  4. Parscostalis - 8-10th costal cart, 11 chostrochondral, 12th (ventral), 13 (dorsal)
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44
Q

What are the 3 opening of the diaphragm and what passes through?

A

Esophageal hiatus between 2 medial division of right crus: esophagus, blood supply, dorsal/vental vagal trunck

Aortic hiatus dorsally vertebral, L/R crucal tendons: aorta, azygos, hemiazygos, lumbar cysterna of thoracic duct

Caval foramen: within central tendon with fused adventia (only imobile of the 3): vena cava

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45
Q

What is the difference between cats and dogs phrenic nn?

A

Dogs: C5-7

Cats: C4-6, 5&6 most important

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46
Q

Described the embyrologic development of the diaphram

A

Transverse septum: central tendon

Dorsal esophageal mesentary (similar to transverse septum: crua, aortic and esophageal hiatus

Pleuroperitoneal folds: lateral portion that completes diaphram, myoblasts invade to form costal mm

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47
Q

What are 2 apporaches for a diaphragmatic hernia?

A

Ceiliotomy

9th lateral thoracotomy - need to know side, containdicated for bilateral or PPHD

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48
Q

WIth taumatic diaphragmatic hernias, what is the distrubution of the tears in dogs vs. cats?

A

Dogs: 40% circumferential, 40% radial, 20% combination

Cats: >59% cricumferential, 18%radial

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49
Q

What is the normal pleuroperitoneal pressure gradient?

A

normal 7-20 cmH20, during maximal inspiration PPG >100mmHg

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50
Q

What is the normal pressure gradient between the liver and vena cava?

A

Portal v: 8-12 mmHG

intrahepatic sinusoids: 3-4mmHg

Hepatic v and cd vena cava 0.5-1mmHg

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51
Q

What are contrast studies that can be used to diagnose a diaphragmatic hernia?

A

oral barium studies

pneumoperitoneography

positive contrast pleurography

portographycholecystography

angiography

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52
Q

What are alternative options of closure of a diaphragmatic defect if primary not possible?

A

Omentum

muscle

liver

fascia

mesh

silicon rubber sheeting

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53
Q

What is the Valsalva effect?

A

decreased venous reuturn from prolonged pulmonary expansion

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54
Q

What are the physiologic effects of compartment syndrome?

A

Decreased renal functoin

hypotension from decreased CO

Hypoxia reduced ventilation and lung compliance

Visceral hypoprofusion

acidosis

ICP

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55
Q

What are 2 types of congential diaphramatic hernias?

A

Pleuroperitoneal

Peritoneopericardial

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56
Q

What are compilcations of PPDH that are not commonly reported with traumatic hernia?

A

RHF, cardiac tamponade, hepatic cysts, gallbladder torsion/rupture, myelolipomatosis, chylothorax.

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57
Q

What are the bounderies of the epiploic foramen?

A

dorsally by the caudal vena cava, ventrally by the portal vein and hepatic artery, cranially by the caudate lobe of liver, and caudally by the celiac artery.

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58
Q

What are the 3 portions of the greater omentum?

A

Bursal (pars superficialis, pars profundus)

Splenic (gastrosplenic lig)

Veil

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59
Q

What are the size of the stomata in the peritoneum?

A

4-16 um mesotheilial process regulate size

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60
Q

What is the classification of peritoneal fluid?

A

Normal: cells <300, protein <3, colloid osmotic pressure 28mmHg

Transudate: cells <1500, protein <2.5g/dL

Modefied transudate: cells 1000-7000, protein 2.5-7.5

Exudate: cells>5000, protein >3

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61
Q

What are factors effecting particulate clearence via lymphatics from the abdomen?

A

Size

gravity

respirtatory and diaphragmatic movement

intestinal activity

Intraperitoneal pressure

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62
Q

What rate can the peritoneal cavity absorb fluid?

A

3-8% of body wt in Kg/ hour

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63
Q

What is normal intra-abdominal pressure?

A

2-7.5 cm H20

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64
Q

What are signs of increase IAP (20m h20) ?

A

increased HR, BP, bacterial translocation

decreased CO, GI blood flow

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65
Q

What are acute phase pro-inflammatory mediators?

What is an anti-inflammatory mediator?

A

Proinflammatory: TNF alpha, IL-8, IL-6, IL-1beta

Anti-inflam: IL-10

Macro produce TNF alpha, IL-1beta ~ recruit neutro, increase prosteglandins

Lymph = IL-6

mesothelial produce IL-8

Mast cell = histamine (+prosteglandin = vasdilation, increased permiability)

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66
Q

List adjuvants in peritonitis.

A

Gastic mucin: inhibits phagocytosis

Bile salts: alter cell adhesion, lyse rbc (increased Hb)

Hb: interferes with chemotaxis, phagocytosis, lymphcytic clearence

Barium

Peritoneal fluid: increased bacterial proliferation, slowed clearence

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67
Q

In dogs vs cats with primary peritonitis, what is the rate of monoclonal bacteria and what kind is present?

A

Dogs: 56% monoclonal, 80% gram +

Cats: 100% monoclonal, 60% gram +

Other organisms FIP, salmonella, chlamydia, clostridium, blasto, mycobacterium, citrobacter

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68
Q

What are indications of a retained surgical sponge on US and cytology?

A

US: hypoechomass with hyperechoic center

cyto: mononuclear cells with mulinucleat giant cells +/- fibers

Particles <15um can be removed by lymphatic circulation

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69
Q

What are causes of aseptic peritonitis?

A

chemical peritonitis

bile peritonitis

uropertoneum

peritoneal FB

starch granulamatous peritonitis

mechanical peritonitis

sclerosing encapsulating peritonitis

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70
Q

What has talcom powder in the abdomen been associated with?

A

Starch granulomatous peritonitis

granulomas, fecal fistula, sinus formation, intestinal obstruction, delayed wound healing

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71
Q

What has sclerosing encapsulating peritonitis been associated with?

A

Steatitis

fat necrosis

finerglass

bacterial peritonitis

chylous effusion

leishmaniasis

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72
Q

GI leakage is the cause of what % of secondary peritonitis in dogs and cats?

A

Dogs: 60%

Cat: 47%

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73
Q

What are possible risk factors after dehisence/peritonitis after GI surgery for incrased mortaliity?

A

longer duration of CS

linear FB

multiple intestinal procedures

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74
Q

How does alpha hemolysin facilitate E.coli and bacteriudes fragilis in septic peritonitis?

A

toxic to cells

decrease pH

lyse rbc

reduces viable leukocytes

presense increases patient mortality and increases likihood of recovery of these 2 species

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75
Q

What is the criteria for SIRIS in 1) dogs and 2) cats?

A

3 or more of these criteria

Dogs: Temp <100.4 >104, HR >120, R >20, WBC <5000 >18,000

Cats: Temp: >103.5, <100. HR >225 < 140. R >40. WBC <5000 >19500. Bands >5%

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76
Q

What is normal sonographic intestinal wall thickness?

A

Dogs:

<20kg: duodenum 4.7mm, jejunum 4.2mm

>20kg: 5.5mm, 4.7mm

Cats:

duodenum 2.7mm, jejunum 2.1mm

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77
Q

How does the accuracy of a single needle tap compare to a pertioneal catheter vs. a DPL for septic abdomen?

A

Needle: 43%

catheter: 83%

Diagnostic peritoneal lavage: 95%

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78
Q

How much fluid is instilled in diagnostic peritoneal lavage?

A

20-22ml/kg

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79
Q

How does serosal patching protect an R&A site and what % does it decrease mortality in patients with colonic perforation?

A

proteolytic activity degrades collagen and ECM

mortality decreased from 82% vs %56

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80
Q

What are advantages of open peritoneal drainage?

A

Increased efficiency removal bacteria

Improved metabolic state

Decreased abominal adhesions

Ease of inspection of abodmen

Unsuitable enviorment for bacteria

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81
Q

How do you diagnose uroabdomen?

A

Cre Fluid > 2.4x serum

Potssium fluid >1.4x serum

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82
Q

What is this?

A

Penrose sump drain

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83
Q

How is enteral feeding beneficial?

A

Good for enterocytes

Decreases bacterial translocation

Decreases mucosal permiabiliyt

Preserves secratory IgA conc in billary secreations

Maintains intestinal structure and function

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84
Q

What are benefical effects of low dose heprin therapy?

A

Improved clotting function

improved bacterial clearence

Decrased fibrin formation

Increased survivial

Decreased abodominal abcess formation

Dose 100-200 U/kg SC TID or QID

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85
Q

What is the mortality rate for septic peritonitis and what are indicators of a poor prognosis?

A

20-70%

Refracotry hypotenision

CV collapse

Resp. distress

DIC

pre-op elevated ALT and GGT

MODS

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86
Q

What is the formula for determining blood volume inthe abdomen from DPL?

A

(Venous PCV)(V in abodomen) = PCV fluid ((V in abdomen) + (V infuse))

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87
Q

What is the nerve supply and vascular supply to the muzzle?

A

nerve CN VII motor, CN V sensory

Facial a = lower lip and cheek

Infaorbital a = uper lip and cheek

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88
Q

What mm. make up the root of the tongue?

A

Styloglossis

Hypoglossus

genioglossus

Innervate by hypoglossal

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89
Q

What is the tube like structure under the tongue (made of mm, fat, cartilage)?

A

Lyssa

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90
Q

Name the gustatory and non-gustatory taste buds.

A

Gustatory: fungiform, vallate, foliate

Non-gustatory: filiform, conical

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91
Q

What are the 3 tonsils?

A

palatine

linguial - tongue

pharyngeal - nasopharx

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92
Q

Describe the 3 phases of deglutinion

A

1. Oropharyngeal

  • oral = bolus CN5, 7, 12
  • pharyngeal = base tongue to pharynx CN9, 10. phayrngeal constrictor mm→food aborally, palatal/pharyngeal mm. close nasopharynx, caudal epigastric reflexion & vocal folds block trachea.
  • pharyngosesophageal or cricopharyngeal = pharynx - circopharyngeal sphinter - eso, CN 9,10. Relax thyropharyngeaus and cricopharyngeaus.
    2. Esophageal - primary parastolic wave +/- secondary wave
    3. Gastroesophageal - muscularis relaxes in front of bolus
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93
Q

Reveiw mm. of tongue and pharynx

A
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94
Q

Borders of the parotid gland?

A

rostral: masseter m. TMJ
caudal: sternomastodideus
ventral: Mandibular SG
superfiical: parotidoauricularis, platysma m

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95
Q

What is the blood supply of the parotid gland, zygomatic gland, M SG, andsublingual SG?

A

Partoid: parotid (external carotid), superficial temporal v., great auricular v.

zygomatic: infraorbital a, deep facial v.

Mandibular: gladular br. of facial a., br. lingual v.

Sublingual:

  • glandular br. facial a (monostomatic)
  • sublingual br. of lingual a. (polystomatic - rostral to lingual n)
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96
Q

What mm. does the SL/Mandibular salivary duct run between?

A

Styloglossis

mylohyoideus

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97
Q

What are the minor salivary glands?

A

Buccal

labial

lingual

tonsillar

palatine

molar (cats - buccal, angle mandibile)

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98
Q

Functions salivary glands?

A

lubricate ingesta

pack food

thermoregulation

oral cavity clensing

buffering week acids

decrease bacteria

protect epithelium

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99
Q

Describe the pathway of saliva

A

intercalated ducts

intralobular ducts

interlobular ducts

lobular ducts

lobar ducts

major excretory ducts

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100
Q

Which salivary glands produce a more mucus secreation?

A

SL/zyomatic - mucus

parotid/mandibular -serous

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101
Q
A
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102
Q
A

A sliding bipedicle flap repair may be used to repair a congenital oronasal fistula. A, The dotted lines represent the mucoperiosteal incisions necessary to create two sliding flaps. B, The mucoperiosteum is elevated from the hard palate with the major palatine artery. C, The nasal mucosa and mucoperiosteum are apposed in two layers over the defect in the hard palate. D, Cross-sectional view of the repair.

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103
Q

A congenital oronasal fistula may be repaired with an overlapping flap technique. A, The dotted lines represent the incisions necessary to allow soft tissue closure. B and C, Elevate the mucoperiosteal flap and rotate it medially to cover the hard palate defect. Insert the edge of this flap between the hard palate and the mucoperiosteum on the opposite side of the defect. Secure the flaps in position with horizontal mattress sutures (inset). D, Complete the repair by apposing the incised edges of the cleft soft palate in three layers. Make lateral relief incisions (broken lines) to reduce tension on the repair.

A
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104
Q

A, Schematic drawing of a repair of a primary cleft palate involving the lip, premaxilla, and nostril. B, Create a flap from the nasal wall and suture it to a labial mucosal flap to separate the nasal cavity from the oral cavity. C, Repair the cleft lip with one or a series of Z-plasties: (1) Make incisions from A to B and a to c; (2) place a suture between A and a, and B and b, to transpose the flaps; (3) place additional sutures as needed.

A
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105
Q

Single-flap technique for fistula repair. A, Incise mucosa around the fistula to create the buccal flap (dashed line), then débride the fistula. B and C, Advance a buccal flap over the defect and suture into place. D and E, After débriding the fistula, create a hard palate rotational flap (dashed line) and rotate the mucoperiosteal hard palate flap over the defect. Suture the flap to surround the mucoperiosteum. F and G, To repair lesions at the junction of the hard and soft palates, débride the defect, then create and close the defect with a soft palate advancement flap (caudal dashed line).

A
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106
Q

A double-layer flap technique may be performed using tissue surrounding the fistula and a flap from the mucoperiosteum of the hard palate. Create the first flap (gingival dashed line) by rotating the gingival margins of the fistula medially and apposing with sutures (top insert). Cover this flap (bottom insert)with a rotational mucoperiosteal hard palate flap (palatal dashed).

A
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107
Q

A double-layer flap technique for fistula repair may be performed using a mucoperiosteal hard palate flap (palatal dashed line) and a buccal flap (buccal dashed lines). A and B, Create a flap from the mucoperiosteum of the hard palate (palatal and gingival dashed lines); rotate and suture to gingival margin. C and D, Cover it with a second flap created from the buccal mucosa (inset), then advance and suture over the first flap

A
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108
Q

Abdominal wall mm. anatomy

A
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109
Q

What is a direct vs. indirect inguinal hernia?

A
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110
Q

Describe scrotial hernia repair when castration not intended?

A

Repair of a scrotal hernia when castration is not intended. A, Proposed skin incision. B, Approach to the inguinal canal by blunt dissection. Evaluation of the hernia contents is made through an incision in the parietal vaginal tunic (hernial sac). The broken line indicates the direction of the abdominal incision if canal enlargement will facilitate reduction or resection of the hernia contents. C, After reduction, a transfixing ligature closes the enlarged vaginal process. D, Simple interrupted suture closure of the abdominal wall, the cranial part of the external inguinal ring, parietal vaginal tunic, and subcutaneous tissues.

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111
Q

Describe en bloc removal of an inguinal hernia?

A

En bloc technique for removal of the hernial sac and macerated hernia contents, thereby reducing contamination at the surgical site. A, Scrotal hernia with necrotic bowel segment. The broken line indicates the proposed skin incision for exposure. B, Ventral midline approach with ligation of the involved vessels, including isolation, transection, and Parker-Kerr oversewing of stumps leading to diseased intestine. Viable intestinal stumps are anastomosed. C, Reduction of oversewn intestine by minimal opening of the hernial ring; simultaneous cross-clamping of the hernial sac neck allows complete removal of the intact hernial sac and autolytic contents.

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112
Q

Describe how to repair a prepubic hernia with mesh?

A

Cuff mesh reinforcement of prepubic hernia. A, Ventral view showing damage and shredding of prepubic ligament. B, Interrupted vertical mattress suture fixation of mesh to the abdominal wall with interrupted sutures placed between reinforced prepubic tendon and pubic bone. C, Completed prepubic repair. D, Double-layer mesh technique to help prevent suture pull-out caused by weak hernia tissue edges

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113
Q

Describe the external oblique release and lateral sheath release.

A

Rectus advancement techniques demonstrating possible dissection planes through abdominal muscle fascia to release tension on a midline defect.

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114
Q

Describe the underlay mesh technique for hernia repair

A

Underlay mesh technique. A, Preplaced horizontal mattress suture catching omentum deep to the folded edge of the mesh. B, Rough edge of overlapped mesh faces away from abdominal viscera. C, Series of preplaced mattress sutures around the defect.

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115
Q

How can the abdomen be divided into quardants or 9 sections?

A

he right and left hypochondriac regions, the epigastric or xyphoid region, the umbilical region, the right and left lateral regions (including the flanks and paralumbar fossae), the right and left inguinal regions, and the pubic region

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116
Q

Structures of the oral cavity

A

General view of the oral cavity of the dog. 1, Vestibule; 2, canine tooth; 2a, philtrum; 3, hard palate; 4, soft palate; 5, tongue; 6, sublingual caruncle; 7, palatoglossal arch; 8, palatine tonsil; 9, frenulum

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117
Q

Frontal section of the head and neck, ventral aspect.

A
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118
Q

Antidrool cheiloplasty. A, Elevate the everted lip dorsally until it is taut when the dog’s mouth is opened maximally. B, Make a 2.5- to 3-cm horizontal, full-thickness incision through the maxillary skin at the site of tautness near the upper fourth premolar, with the caudal edge of the incision ending at a line parallel to the medial canthus and the caudal labial commissure. C, Remove a 2-mm wide strip of mucosa 2.5-cm long from the mucocutaneous junction of the lower lip, beginning 2 cm rostral to the commissure. D, Create 0.5- to 0.75-cm flaps. E, Evert the flaps through the skin incision, using a hemostat or stay sutures to grip the flap. F and G, Secure with vertical mattress sutures. Dashed line (F) represents the mucosal flap from the lower lip

A
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119
Q

What are phases of excretion of saliva?

A

Phase 1:

  • acinus make saliva, (cells absorb Na, draws in water, Na rich)

Phase 2:

  • intralobular duct epithelium: resorb Na, secreate bicarb and K
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120
Q

What does parasympathetic stimulation do to saliva production?

A

Increase

= blood vessel dialation and stimulation of cGMP ⇒ upregulate acinar cell activity

Via facial n. and mandibular nn.

sympathetic = minor inhibition after initial myoepithelial cell contraction

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121
Q

What are non-surgical disease of salivary tissue?

A

Sialoadenosis - treatment phenobarbital, limbic epilpsy

  • esophageal abnormalities may also be present (sx, abx, and steriods do not help CS)

Sialoadenitis - terrier breeds predisposed

  • possible link to hyperstimulation of the vagas n. = neural reflex syndrome
  • may have similar cause as sialadenosis, some respond to phenobarb
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122
Q

Leakage from which salivary gland is most common?

A

Sublingual SG and duct

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123
Q

What dog breeds are predisposed to sialoceles?

A

poodles, GSD, Australian silky terriers, dachshunds

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124
Q

What are the 4 kinds of sialoceles?

A

Pharyngeal - caudodorsal or lateral pharynx, rostral to epiglotis = dsypnea

Zygomatic - orbital swelling, exopthalmous, elevated 3rd eyelid

Sublingual

Cervical

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125
Q

What is a stain that is specific for mucin?

A

Periodic acid-schiff

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126
Q

What is a differential dx for cervical mucocele?

A

Brachial cleft cyst - has true secretory lining

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127
Q

What is the recurrence rate of siaocele post sx removal?

A

5%

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128
Q

What are possible treatment strategies for sialoliths?

A

gland/duct removal

duct ligation

duct R & A

duct marsupialization into the mouth

incision over the stone +/- repair

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129
Q

Where are sialoliths most commonly found?

A

Parotid duct

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130
Q

What % of dogs and cats had regional lymph node involvement for sialoliths?

A

Cats: 39% regional, 16% distant

Dogs: 17% regional, 8% distant

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131
Q

What is the prognosis for salivary neoplasia?

A

MST 74-550d

correlated with stage, not grade

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132
Q

Describe approach to removal of the zyogmatic salivary gland

A

horizantal incision over dorsal aspect arch

Aponeurosis of masseter m. reflected ventrally

Orbital fascia reflected dorsally

remove portion of the arch

dissect gland - ligate br. infraorbital a. (malar a.)

do not repalce bone

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133
Q

Describe the approach to the parotid sialoadenctomy.

A

Incise over vertical ear canal (level fo the acoustic meatus) to angle mandible

incise platysma and parotidoauricularis m

ligate caudal auricualr v.

ligate duct

remove accessory parotid SG dorsal to the duct

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134
Q

What are the orgin and attachments of the major mm of mastication?

A

Masseter: zygomatic arch → lateral surface caudal body/ramus

Tempoalis: temporal skull → dorsal ramus

Pterygoideus: pterygoid, palatine, sphenoid bones → angular process

Digastricus (open): occiptal skull → ventral body

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135
Q

What is the blood supply of the mandible?

A

Maxillary a. → mandbiluar foramen → mandibular alveolar a. → mental foramen

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136
Q

Nervous supply of the mandible

A

Trigeminal n. → mandibular foramen → mandibular alveolar n. (sensory) →mental foramen →mental n. (incisors)

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137
Q

What are the 3 bones of the maxilla?

A

Maxilla: canine through molars

Incisive/premaxila: incisiors

Nasal: dorsal midline

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138
Q

What is the blood supply to teh maxilla?

A

Maxillary a → major palatine a. → caudal palatine foramen

Maxillary a. →maxiallary foramen → infraorbital a. → infraorbital foramen

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139
Q

What is the innervation of the maxilla?

A

CN 5 → maxillary n. →infraorbital canal

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140
Q

Muscles of the mandibule and blood supply

A
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141
Q

What are the 5 most common oral tumors? and what breeds are associated?

A

Melanoma: cockers, poodles, chows, goldens (small breeds)

SCC: older large breeds

FSA: middle to older large breeds: labs, goldens

OSA: medium to large breeds

Acanthomatous ameloblastoma: medium to large breeds

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142
Q

What are the 3 epulidides and their origins?

A

Acanthomatous: odontogenic epithelium

Fibroumatous eplis: peridontal lig.

Ossifying epulis: unknown

The last 2 can be cured with local excision, no bone removed

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143
Q

What percent of gingival bone tumors causes radiographic osteolysis?

A

60-80%

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144
Q

How does lymph node size relate to metastasis?

A

Inaccurate for metastatic disease

sens 70%, spec 51%

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145
Q

What are different types of mandibulectomeis?

A
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146
Q

What is the general prognosis for oral tumors?

A

70-90% 1 year survival with aggressive surgery

local recurrence <50% usually much less

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147
Q

What aspects of oral tumors are associated with a worse prognosis?

A

tumor type - melanoma and OSA worse bc malignant

Location - caudal location

incomplete excision: local reccurence complete ~20%, incomplete ~65%

Overall recurrence rates and survival best for SCC and ameloblastoma

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148
Q

What are the most common feline oral tumors?

A

SCC - 20-30% have nodal metastasis

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149
Q

What is the prognosis for feline SCC: mandibulaectomy +/- RT?

A

Mandibulectomy: progession free survival 56% 1yr, 49% 2yr

  • 48% incomplete, 43% recurrence

RT alone MST 3 months

Mandibuletomy + RT = MST 14m 86% local recurrence

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150
Q

What are the 4 layers of the esophagus?

A

Adventitia

Muscularis - striated in dogs, caudal 1/3 smooth cats: arises from cricopharyngeus m and cricoesophageal tendon

Submucosa

Muscosa: stratified squamous epithelium

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151
Q

What composes the upper and low esophageal sphincters?

A

Upper: thyroipharyngeus, cricopharyngeus

Lower: thickended circum. striated mm, diaphragmatic crua, anlge meets stomach and the fold of the gastroesophageal mucosa

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152
Q

What is the blood supply of the esophagus?

A

Cerival: cranial and caudal thyroid aa.

Crainal 2/3 thoracic: bronchesophageal a.

Caudal: esophageal br arota or intercostal a

Terminal portion: left gastric a.

Venous: cervical external jugular vv. , thoracic azygous v.

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153
Q

What is the nervous supply of the esophagus?

A

branches of the vagus nn.

  • paried pharyngeal esophageal nn
  • recurrent laryngeal nn.
  • paralaryngeal n.
  • dorsa and ventral vagal trunks
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154
Q

How do you do a hemi-mandibulectomy?

A

Total hemimandibulectomy. A, Position the patient in ventral recumbency. B, Incise the mucosa 1 to 2 cm from the lesion. Incise the commissure to allow better exposure of the caudal mandible. Separate the mandibular symphysis and identify and transect (broken line) the muscles. C, Dissect and transect the lateral mandibular muscles and expose the temporomandibular joint. D, Dissect and transect the medial muscles of the mandible and identify the mandibular artery entering the mandibular foramen. Ligate the mandibular vessels, disarticulate, and remove the mandible. E, Appose the buccal and sublingual mucosa with approximating sutures

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155
Q

What are the transit times through the cervical esophagus?

A

Liquid in sternal: 2.54 cm/sec

Liquid in lateral: 7.23cm/sec

Kibble in sternal: 4.44cm/sec

Kibble in lateral: 8.92cm/sec

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156
Q

Reflex control of swollowing

A
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157
Q

What are potential reasons that the esophagus has a higher dehisence rate?

A

lack of serosa (elaboration of fibrin seal, source pluripotent mesothelial cells)

segmental blood supply

lack omentum

comstant motion

tension at site

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158
Q

What happens if disrupt segmental blood supply?

A

Can disrupt throacic if cervial and abdominal intact

disruption of cerival and thoracic = necrosis at inlet

most ischemic necrosis due to intramural vascular supply damage

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159
Q

What sx appraoches should be performed to reach the cervical, cr. thoracic and caudal esophagus?

A
  • Cervical ventral midline
  • Left 3-4 intercostal (brachiocephalic trunk and subclavian ventallly), right 3-5 intercosal (ventral trachea, ligate/retract azygous v.)
  • left 7-9 (avoid vena cava and dorsal/ventral vagus nn)
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160
Q

How is the esophagus sutured and with what type of suture?

A

polydiaxonone or polyglyconate

2mm from edge and 2mm apart

single layer simple interrupted, continous (worse wound strength and apposition) and double layer interupted described. interrupted prefered and double layer seems standard.

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161
Q

How much esophagus can be removed in an R&A?

A

Clinically >3-5cm increased risk dehisence

Experimentally 20% of cervical esophagus or 50% thoracic esophagus

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162
Q

Describe how to do an a circimferential partial myotomy for esophageal R&A.

A

Outter longitudial layer incised 2-3cm cranial or caudal to R & A. If inner muscular incised = damage to submucosal vascualr plexus and necorsis

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163
Q

What was the mortality rate and complications with stapler and biofragmentable anastomsis ring devices?

A

No difference in complication rate or healing between the 2 devices

  1. 3% mortality rate - all biofrag
  2. 3% leak - all biofrag

11% stricture - all stapler

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164
Q

What are 2 types of esophageal patching?

A

inlay = partial circumferntial replacement

onlay = reinforce primary closure dt tension/decreased vascularity

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165
Q

What are materials that can be used for patching?

A

Omentum = mimize stricture formation → need to ligate right gastroepipolitc a.

Pericardium = increase strength without increased risk stricture

Local muscle flaps: sternohyoideus, longus coli (decrease stricture formation), free buccal mucosal graft, vascularized pedicle graft of internal/external intercostal mm (elevate periosteum), diaphram pedicale graft

Stomach, Jejunum (post mucosal stripping)

Lung

Porcine SIS, lyophilized dura mater, collagen coated vicryl mesh, expanded polytetrafluroehtylene patches

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166
Q

What are some options for esophageal substitution?

A

Cervical:

  • Inverse tube skin graft: crainally based pedicle, inverted tube, sutured to distal esophagus, 2-3 weeks later cut pedicle. ALT: suture cranial and caudal esophagus to skin and 3-4 weeks later make tube.
  • omocerival cutaneous island axial pattern flap - one stage tube skin graft
  • possible complications; obstuction with hair, lack peristalsis and indistensibility

Thoracic:

  • tubed inercostal musculopleural pedicle graft
  • diaphragmatic pedicle graft
  • tub lat dosi flap based on thoracoforal vessels
  • gastric advancement and esophagogastric anastomosis
  • isoperistalitc and antiperistaltic gastric tubes from greater curvature stomach (splenectomy required, consider pyloromyoplasty to enhance emptying since likely disrupt vagal innervation)
  • jejunum (free microvascular graft)
  • colon: more tolerent to ischemia than jejunum
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167
Q

What is the normal embryonic fate of the arches?

A

Ventral arotas = (1-2) external carotid aa, (3-4) common cartid aa.

Dorsal arotas = (1-2) internal carotid aa., (3-4) involution, (>4) desecending aorta

Left and right 1&2 = involution

Left 4th root/arch = adult arotic arch

Right 4th root = brachocephalic trunk

Right 4th arch = right subcalvaian a.

Left and right 5th = involuation

6th = pulmonary aa., left pulmonary retain connection to arota (left ductus arteriosus = ligamentum areriosum)

Left 7th intersegmental a = left subclavian a.

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168
Q

What are the most common vascular ring anomalies?

A

PRAA + left ligmentum ateriosum (C)

PRAA + aberrent left subcalvian= incomplete ring = (described with both left LA (2 structures) or right LA(single structure (G,F)

Double AA = both aortic arches persist, trachal stenosis (D)

Persistent right LA with normal left AA (mirror image PRAA) - cannot do left thorcotomy to correct (E)

Aberrant right subclavian a with normal left AA (incomplete ring) (H)

Persistent left cr. vena cava with non-elastic band around esophagus

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169
Q

What are vascular ring anomalies in cats?

A

PRAA with left LA

PRLA with left AA
PRAA with right LA and aberrent left SC
double AA

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170
Q

What is the general % of congenital abnormalities in dogs and cats/

A

Overall 20% - most not clinically sig.

Aberrant right SC most common, 6% - not clinically sig

95% clinical cases PRAA with left LA,

Ductus arteriosis patent in 10% with PRAA

Persistent left cr. vena cava in 45% - complicate approach

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171
Q

What breeds are predisposed to VRA?

A

Irish setters, GSD, breeds >15kg

siamese, persians

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172
Q

What is the prognosis for VRA?

A

No difference if operated early or late, survival at 2 weeks 92%, maybe good with some persistence of megaesphagus

Factors that effect prognosis include:

  • degree of esophageal dialation
  • severity of debilitation
  • presence of aspiration pneumonia
  • medical management before and after surgery
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173
Q

What breeds are effected by generalized megaesophagus and what is the suspected underlying cause?

A

Irish setters, GSD, danes, labs, shar-peis, newfies, mini schanauzers, fox terriers

defect in vagal afferent innervation

74% dead by 1 year age

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174
Q

What is a possible sx treatment for congenital megaesphagus?

A

Esophagodiaphargmatic cardioplasty - pulls caudally on esophagus during respiration

Good outcome in 50%

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175
Q

What is a esophageal duplication cyst?

A

Often fluctuant mass cranioventral cervial region

2 muscle layers and epithelium

Can excise with good outcome

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176
Q

Where do esophageal foreign bodies generally lodge for bones, fish hooks and dental chews?

A

Bones: heart- diaphram 65-79%, heart base 11-39%

Fish hooks: pharyngeal esophag 34%, thoracic inlet 11%, heart bse 30%, heat-diaphram 5%

Dental chews 74% in distal esophagus

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177
Q

What are reasons for surgical removal of an esophageal forgein body?

A

Inability to remove endoscopy: 63% remove with endo, 29% pushed into stomach, 8% need sx

If contrast migrates away (if compartamentalized around perf can med mang)

pleural effusion

pneumothroax

pneumomediastinum

sepsis

endoscopic risk laceration

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178
Q

What is the prognosis for penetrating forgein bodies?

A

Mortality rate 26% with stick penetration

acute penetrating FB worse that oropharyngeal pentration

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179
Q

What percent of post-anesthesia esophageal strictures are single or multiple?

A

Single 62-75%

Multiple 38%

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180
Q

What is the difference in force between bougienage or ballon dialation?

A

Bougies - longitudinal shear

Balloon - radial force

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181
Q

What is the incidence of perforation for ballon dialtion and bougienage of the esophageal strictures?

A

Balloon = 3.6-11%

Bougienage 3.6%

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182
Q

What are options for treatment of esophageal strictures?

A

bougienage

balloon dialation

steroids (oral/intralesional) - no evidence

Esophageal stents

Surgery: esophagoplasty - transverse closure, esophageal R&A, patch esophagoplasty - (incise longitudinally and inlay sternohyoid, incostal, diaphram, or pericardium), esophageal substitution

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183
Q

What is the prognosis for general treatment of esophageal stricutre?

A

Good: 71-88%

Surgery associated with high rate of stricture recurrence and dehisence

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184
Q

What are 3 types of esophageal diverticulums?

A

Pulsion: outpouching of mucosa through tunica muscularis

traction: full thickness deviation (assumed from inflammation of adjacent organ)

Epiphrenic: between heart base and diverticulum

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185
Q

What percent of canines with an esophageal diverticulum had a bronchoesophageal fistula?

A

50%

If impacted

→ obstruction

→chronic esophagitis → stricture

→ peridiverticulits → adhesion/fistula

→ rutpure

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186
Q

What breeds tend to get an esophageal diverticula?

A

Small breeds

Cairn terriers (propensity for FB??), mini poodles, Parson Russel terriers

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187
Q

How are esophageal diverticula treated?

A

Small diverticula: conserative, guel diet

Large: lateral thoracotomy

Excision via stapler, partial resection and in-lay, complete R&A, esophageal substitution

PX: good for simple, guarded for extensive repair

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188
Q

How is a congenital esophageal fistulae caused?

A

Incomplete separation of the tracheobronchial tree from the digestive tract

aquired due to FB

Bronchoesophageal > tracheoesophageal

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189
Q

What is the most common lung lobe effected by esopheal fistula?

A

Right caudal (66%)

Others: right cranial, middle, accessory and left caudal

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190
Q

What is cricopharyngeal dysplasia?

A

Swallowing disorder characterized cricopharyngeal achalasia or asynchrony

Usually congenital and dx by 12 m, older may be aquired

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191
Q

What cricopharygeal achalasia? asynchrony?

A

Achalasia: upper esophageal sphincter fails to open during cricopharyngeal phase

Asynchrony: incoordination between contraction of pharyngeal contractor mm. and relaxion of upper sphincter

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192
Q

What is the treatment for cricopharyngeal dysphagia?

A

CP myotomy or myectomy

Ventral or lateral approach

Place orogastric tube, remove 2cm of m. → place metal clips for post-op fluroscopy

Also described with thyropharyngeal myotomy

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193
Q

Descrine the origin, insertion and innervation of the criopharyngeal m.?

A

Singel muscle

Origin: lateral surface of cricoid cartilage → spreads over esophagus → attaches on other side.

Innervation: CN9 (glossopharyngeal n.) and pharyngeal br. of vagus n.

Blood supply: cranial thyroid a.

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194
Q

How do you differeniate pharyngeal dysplasia from criocopharyngeal dysphagia?

A
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195
Q

barium study for CP dyplasia

A

Lateral fluoroscopic view of barium swallow. Barium appears black on fluoroscopy. Row 1, Normal dog; 1A, liquid barium bolus in the pharynx; 1B, closure of the epiglottis at the onset of swallowing; 1C, opening of the cranial esophageal sphincter; and 1D, closure of the cranial esophageal sphincter and reopening of the epiglottis. Row 2, Dog with cricopharyngeal achalasia; 2A, liquid barium bolus in the pharynx; 2B, contraction of pharynx without opening of the cranial esophageal sphincter; 2C, opening of cranial esophageal sphincter and reopening of the epiglottis; and 2D, closure of the cranial esophageal sphincter.

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196
Q

Lateral approach to the pharynx

A
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197
Q

What is the prognosis for CP dysplasia?

A

Complete resolution CS in 49% dogs, another immediate resolution in 13/14 dogs

Poorer px: failure to transect all bands, incorrect diagnosis, concurrent pharyngeal/esophageal dysfunction, structural problems (fibrosis), esophageal stricture, function disease, masticatory myosti, myasthenia gravis, aspiration pneumonia, malnutrition

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198
Q

What the most common esophageal tumors in dogs and cats?

A

Dogs: SCC leiomyosarcoma, ODA, FSA < sarcoma, leiomyoma, plasmacytoma

  • most common site caudal esophagus

Cats: SCC

  • most common site cranial thoracic esophagus
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199
Q

What parasite is associated with esophageal nodules in dogs?

A

Spirocerca lupi

Dogs definative host: ingest coprophagous beatle → larvea gastric mucosa to aa. → thoracic aorta wall to caudal esophagus

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200
Q

What tumors are associated with Spirocerce lupi?

A

OSA, FSA, undiffereniated sarcoma

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201
Q

What are clinical signs assocaited with maligant spirocera tumors?

A

HO 38%, none with benign had

Lower Hct, higher WBC and platelets

Malignant masses larger (6x7cm) and more likely to cause bronchia displacement (52% vs 17%)

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202
Q

Diagnostic findings consistent with spirocera?

A

Microcytic anemia

Rads: masses, mets, HO

Caudal thoracic spondylitis and aortic mineralization

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203
Q

What % of esophageal tumors have mets at diagnosis?

A

50%

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204
Q

Name important structures of the stomach.

A

4 parts: cardia, fundus, body, distal 1/3 (pylorus (double mm layer) , pyloric antrum, pyloric canal)

Cardiac notch: btwn cardia and blind outpouching of stomach

Angular incisure: where papliary process of liver lies

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205
Q

Describe the blood supply of the stomach

A

Celiac a.

  1. splenic → pancreatic and L. gastroepipolic (greater curve, anastoms with R. GE) , short gastric aa.
  2. Hepatic → br. to liver and gallbladder
    1. Right gastic → pylorus
      1. Gastroduodenal
        1. Right gastroepipolic
        2. Cr. Pancreaaticoduodenal
  3. Left gastric → lesser curvature

Portal v.

  1. Gastroduodenal → Right, gastric, R. gastroepiploic
  2. Gastrosplenic → Left gastric, Left gastroepipolic
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206
Q

What is the innervation to the stomach?

A

Parasymphatheticvagus n. → ventral vagal truck (pylorus, liver, lesser curve), dorsal vagal (lesser curve, ventral wall → then follows celiac and cr. mesenteric a.)

Sympatheticceliac plexus (arise from celiacomesenteric plexus and follow gastric br celiac a)

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207
Q

Describe the gastric layers.

A

Serosa

Muscularis

  • Circular = cardia to pylorus except fundus, Longitudinal = esophagus to pylorus on greater curvature (not lesser, ventral and dorsal body), Fundus and body = inner oblique fibers

Submucosa

Mucosa

  • Columnar surface epithelium, Glandular lamina propria and Lamina muscularis mucosa
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208
Q

Describe the locations and gland types of the stomach.

A

3 types: cardiac, pyloric and gastric.

Cardiac (cardia and antrum): serous

Pyloric (pylorus and gastric body): mucus

Gastric (fundus and body):

  • Parietal
  • Cheif
  • Mucous neck
  • endocrine
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209
Q

Describe the functions of the gastric cell types:

A

Parietal (oxyntic):

  • maintain gastric acid pH (pump H+ into lumen), allows activation of gastric enzymes food breakdown
  • produce intrinsic factor: mucoprotein that binds to B12 to allow absorption SI

Cheif: pepsinogen → converts to pepsin (protein breakdown)

Mucous: mucous to protect glandular cells from acid and enzymes

Endocrine: gastrin, histamine, serotonin

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210
Q

Describe the different mechanisms of healing in the stomach

A

Superfical: epithelial migration

Mucosa erosions: epithelial regeneration

Injury to submucosal = ulcer

  • short-term fibrous protein synthesis > wound contration and scar resorbed
  • long-term: exuberant fibrotic repair with permanant scar

Incisional healing:

  • similar to other areas: inflammation, debridment, repair, maturation
  • In contrast other tissue, GI smooth muscle contribute to collagen production
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211
Q

What is the downside to withholding food 8-12 hours prior to sx?

A

Decreased gastric pH = increased GE reflux (57% ortho procedures, 14% clinically noted. In post-anesthesia esophageal dysfunction, only 46% clincially noted)

Doesn’t reliably decrease contents

May help to feed small amounts q3hr

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212
Q

What anesthestic agents may be beneficial for gastic sx?

A

Anticholingerics - decreased gastic secreations

H2 blockers

AVOID nitrous = rapid diffusion into gas filled organs

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213
Q

Transection of which lig. may help with exposure of the stomach?

A

Hepatogastric

hepatodoudenal

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214
Q

What is a disadvantage of flush that is warmer than normal body temp?

A

Increase body temp

vasodilation/hypotension

increased adhesion formation

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215
Q

Describe paracostal approch to stomach

A

In rare instances when exposure of only a portion of the stomach is required, a paracostal approach may be used. A paracostal approach is achieved by making a curved incision approximately 2 cm caudal to the last rib. The underlying muscle layers, including the external and internal abdominal oblique and transversus abdominis muscles, are split longitudinally along the direction of the muscle fibers. When ventral extension of the incision is necessary for visualization, the rectus abdominis muscle may require transection. Closure is achieved with a simple continuous pattern in each muscle layer

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216
Q

What is the half life of PDS, maxon and monocryl in gastric fluid?

A

PDS: 12d - only suture tensile strength effected, @ 2pH 10x shorter than at 7.4

Monocyrl 15d

Maxon 75d

Polyglycolide and poly l-lactidie coglycolide had inital delays in linear absorption = coating

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217
Q

What staples have been reported for stomach closure? And pexy?

A

TA, GIA, skin stapler (oversew of line recommended)

Pexy: GIA or skin staples (with skin staples tensile strength similar to belt loop)

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218
Q

What are methods of determining viabillity of the stomach?

A

Subjective (85% accurate): Wall thickness, perastalsis, serosal capillary profusion, serosal color

  • incise seromuscular layer = evaluate a. blood supply

Objective:

Fluorescein dye injection: 58% accurate

Lazer flow doppler = to subjective

Scintigraphy: 79%

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219
Q

List types of gastropexy.

A

Incisional - 4-5cm, parralel or perpendicular to long axis

Belt-loop

Circumcostal - double or single hinged

Incorporating - no inicison in stomach

Tube gastropexy - highest recurrence rate 5-29%

gastrocolopexy - nonabsorbable suture, scarified/not incised

Lap/Lap-assited

Endoscopically assicsted

Grid approach - mini-lap

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220
Q

What is a Fredet-Ramstedt myotomy? Disadvantages?

A

Longitudinal seromuscular inision through the pylorus

Does not allow: visualization gastric mucosa, relieve restrictions of the mucosa/submucosa, provide full thickness biopsy

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221
Q

What is a Heineke-Mikuliez pyloroplasty?

A
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222
Q

What is a Y-U pylorplasty?

A
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223
Q

What are indictions for a bilroth 1?

A

Neoplasia confined to pyloric region

Ulceration of outflow track

Pyloric hypertrophy

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224
Q

Describe technique for Bilroth 1.

A

Pylorectomy with end to end gastroduoenostomy

No difference in leakage between a single and double layer closure

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225
Q

What is the prognosis of a bilroth 1?

A

75% survive 2 weeks, but only 33.3% alive at 3 months

Complications:

  • 63% hypoalbuminemia
  • 58% anemia
  • Decreased survial with preop weight loss
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226
Q

What is a bilroth 2?

A

Partial gastrectomy with gastrojejunal anastomosis

(duodenum and gastrotomy close, jejunum anastomsed to the side)

poor results

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227
Q

What is the classification system for hiatal hernia?

A

I: sliding hernia: intermittent movement GE junction into thoax, congenital common (Shar peis and English bulldogs). Aquired = BAS or upper resp. disease

II:Paraesophageal: GE junct normal postion, fundus herniated

III: Elements both I and II

IV: herniation of other organs besides stomach

A, Normal anatomy of the junction of the esophagus and stomach. B, Type I sliding hiatal hernia in which the gastroesophageal junction has moved cranial to the diaphragm. C, Type II paraesophageal hernia occurs when a portion of the stomach moves into the caudal thorax through the hiatus adjacent to the esophagus. D, Type III hiatal hernia combines the movement of the gastroesophageal junction into the thorax as well as movement of a portion of the stomach into the thorax adjacent to the esophagus. E, Gastroesophageal intussusception.

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228
Q

What are the goals of medical management of hiatal hernia?

A
  1. Reduce gastric acid: H2 blockers and proton pump inhibtors
  2. Esophageal mucosas protection: sucralfate (polyaluminum sucrose - binds denuded mucosa)
  3. Increase gastric emptying: prokinetics, low fat diet in elevated postion (if megaesophogus)
  4. Enhance LES tone: prokinetics
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229
Q

How many hiatal hernias improve with medical management? And how long should it be attempted prior to surgery?

A

53% (8/15)

recommend for 30 days

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230
Q

How is hiatal hernia treated surgically?

A
  1. Phenoplasty = Phernicoesophageal lig. transection OR horizantal mattress sutures with nylon 2-0. Alone = reherniation
  2. Esophapexy: left esophagus to diaphram
  3. Gastropexy: left body wall (increases LES tone)

Before performing need to transect the hepatogastic lig. and place orogastric tube

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231
Q

Describe the cause, breed, presentation and treatment of gastroesophageal intussusception.

A

Suspect esophageal abnormalitis (megaesophapgus), abnormal esophagus motility, laxity of hiatus

>50% GSD, >75% less than 3 months

Severe respiratory compromise and GI signs

EMERGENCY - Left and right gastropexy

Mortality rate 95% (1984), improved, life long management esophageal abonormalities and aspiration pneumonia

232
Q

What is hyperthrophic pylogastropathy?

A

Pyloric senosis. Bas → air=increased gastric pressure →increased gastrin, gastic acid = increased cholecystokinin and secretin → antral and pyloric mucosal hypertrophy

Congential: BAS, <1yr Aquired: small breed

Treat with pylortomy, pyloroplasty, Y-U pyloroplasty = only plasty techniques have been shown to increase gastric emptying and allow full thickness biopsy to rule out neoplasia

Px: good >80% improve (ie no chronic vomiting)

233
Q

How to dx hypertrophic pylorogastropathy?

A

Retention gastric contents > 8 hours

Apple core appearence with contrast rads

endo biopsy to rule out neoplasia

234
Q

What percent GI foreign bodies are gastric and what is the most common electorlyte abnormalitiy

A

16-50% in stomach

50% of GI FB are HYPOchloremia

235
Q

What are the most common GI tumor types in 1) dogs and 2) cats?

A

Dogs: adenocarcinoma

Cats: LSA

Others: LSA, FSA, gastric medullary plsmacytoma

236
Q

What percent of tumors are adenocarcinomas, breeds predisposed and percent mets?

A

42-90% of gastric tumors (usually pyolurs or lesser curvature)

Mets 70-80% - lungs, nodes, liver

Males, Belgian shepards, rough coated collies, staffies

237
Q

How can differentiate leiomyosarcoma from GIST?

A

GIST c-kit positive

GIST from interstital cells of Cajal

238
Q

What is the MST of GI lymphoma in dogs?

A

17 days :(

239
Q

What is the MST of pythium?

A

MST 26 days

Gastric outflow most commonly effected

240
Q

What are causes of gastric ulceration?

A

hepatic/renal disease

neoplasia

NSAID

Steroids

decreased blood flow, increase gastric acid, decrease proteglandin, decreased mucus/bicarb

241
Q

How does hepatic/renal disease cause gastric ulceration?

A

Renal = hypergastrinemia from decreased clearence or increased secreation gastrin

Hepatic

  • decreased degradtion of gastrin and histamine → increased gastric acid secration
  • Portal hypertenision → derangement of mucosal blood flow
242
Q

How do NSAIDs cause GI ulceration?

A
  1. Direct topical effect - weakly acidic, lipid soluable
  2. Cox → decreased protective PG → decreased blood flow, epithelial mucus production, bicarb, epthelial turnover
    - (Cox 2 doesn’t alter PGE1 and E2 but linked to slower gasric mucosal healing)
    - overall combination of COX 1&2, interaction of NSAID with phospolipids and subsequent uncoupling of mitochondrail oxidative phosphorylation
243
Q

H2 antagonists

A

least potent: cimetidine q8 < ranitidine q12 < famotidine q24

cimetidine inhibits p450 → may interfere with metabol other drugs

ranitidine: prokinetic

244
Q

How do proton pump inhibitors work?

A

Covalent binds H+/K+ ATPase = block secreation H+

Absorbed in alkaline enviroment: proximal duodenum

metbolized by p450

adminster 1 hr before food, complete inhibition of gastric acid secretion in 3-5 ays

245
Q

How does sucralfate work?

A

Sulfated diasaccide -aluminum hydroxide complex

Acid→ sucralfate dissociates to sucrose octosulfate → polymerize to thick substance that binds electrostacially charged proteins (ulcer base)

Prevents back diffuse of H+ ions, inactivates pepsin, absorb bile acids

Stimulate PG release locally

246
Q

How does misoprostal work?

A

Synthetic analog of PGE

increases bicarb secreation, mucus production, mucosal blood flow

decreases cAMP → decreases H/K ATPase pump activity → decreased acid secreation

half life 30 min, give 4 x daily

inhibits ulcer formation but doesn’t heall

247
Q

What tumors are associated with gastric perforation?

A

Gastrinoma and systemic mastocytosis

Gastinoma: non-beta pancreatic islet cell tumor → hypersecreate gastrin from antral G cells → gastric hyperacidity/ulcers

248
Q

What direction does the stomach rotate with GDV?

A

pylorus moves ventrally and cranially

Stretches hepaticoduodenal ligament

249
Q

What are risk factors for GDV?

A

1st degree relative with GDV

increased thoracic depth:width ratio

feeding fewer meals, small particle size, exercise post meals, rapid eating

aggressive temperment

increased hepatogastric lig

250
Q

What breeds are predisposed to GDV?

A

Gordan and Irish setters,

Poodles

St. Bernards

Weimies

Bassetts

Danes

251
Q

Describe pathophys of GDV

A

Blood supply:

  • Increase IAP → CVC and portal v. → decrase return blood to heart and portal hypertension → increased bacterial translocation (although no difference btwn control) and decrease liver clearence bacteria (decrease endoreticular funct.
  • increase pressure diaphragm → decrease O2
  • increase intragastric pressure → stomach mucosal and wall necrosis

Cardiac disease:

  • myocardial ischemia → arrythmias, mycardial depressent factor

Reprofusion injury

252
Q

What percent of GDV have ECG abnormalities?

A

40-70%

Cardiac troponin peak at 48-72hr and correlates with arrythmia severity

253
Q

How do lactate measurements corrleate with necrosis and survival for GDV?

A

Necrosis: >6mmol/L → 61% sens, 88% spec

Survival:

> 6 58%, <6 99%

>9 54%, <90%

if >9 response to therapy was predicitve:

>4 change → 86% survival

>42.5% percent change → 100% survival

final value <6.4 → 91% survival

254
Q

What are the recurrence rates for various gastropexys?

A

Circumcostal gastropexy 4-7%

belt loop: none

Gastrocolopexy: 3/20 (15%)

Incorporaing: 4/61 (7%) → GD died/euth

255
Q

Mechanical testing of gastropexy

A

Circumcostal: strength N 109, 21d post test

Belt loop: strength N 109, 50d post test

Incisional: 60, 62, 85. 21d, 58d, 30d

Laproscopic: 45, 77, 106. 30d, 50d, 30d.

256
Q

What is the survival rate GDV and factors that decrease survial?

A

73-90%

Increased duation signs >6h, gastrectomy/splenectomy, hypotension, arrythmias, peritonitis, sepsis, DIC, lactate, myoglobin

Myoglobin: <168ng/mL 60% sens, 84% spec = 50% above died, 90% below survived

Bacteremia NOT associated with survival

257
Q

How does prophylactic gastropexy effect life time risk gastropexy?

A

Lifetime risk in risky breeds: 4-37%

29 fold decrease mortality rate with prophylactic

258
Q

Describe adhesion strength gastropexy

A

Similar for circumcostal, belt loop, incisional and lap-assited.

Stapler for total lap: weaker first 7 days, then no diff at 30d

259
Q

What is the nervous supply to the small intestine?

A

splanchnic n. via celiac and cranial mesenteric plexus

vagas

Abdominal autonomic nervous system, left lateral view. The cranial mesenteric ganglion (34) is located on the sides and caudal surface of the cranial mesenteric artery. 1, Stomach; 2, ventral trunk of vagus nerve; 3, esophagus; 4, dorsal trunk of vagus nerve; 4a, celiac branch of dorsal vagal trunk; 5, aorta; 6, intercostal artery and nerve; 7, ramus communicans; 8, sympathetic trunk; 9, celiac artery; 10, quadratus lumborum; 11, major splanchnic nerve; 12, cranial mesenteric artery; 13, lumbar sympathetic ganglion at L2; 14, minor splanchnic nerve; 15, tendon of left crus of diaphragm; 16, psoas major; 17, lumbar splanchnic nerve; 18, transected psoas minor; 19, deep circumflex iliac artery; 20, caudal mesenteric artery; 21, left hypogastric nerve; 22, caudal mesenteric plexus; 23, caudal mesenteric ganglion; 24, testicular artery and vein; 25, descending colon; 26, cranial ureteral artery; 27, jejunum; 28, caudal vena cava; 29, greater omentum; 30, renal artery and plexus; adrenal gland; 32, common trunk for caudal phrenic and cranial abdominal vein; 33, adrenal plexus; 34, celiac and cranial mesenteric ganglia and plexus.

260
Q

What are the 2 types of contractions in the SI?

A

Semental: strech reflexes and vagas - mix food

peristaltic: migrating myoelectricl complexes
- cycel every 1.5-2h in periods between meals and pylorus opens during this time to let indigestible things pass

261
Q

Describe the general transport mechanisms and water absorption.

A

Active = sodium pump and N-K-ATPase, against conc. grad

Passive= with conc grad.

  • Facilitated: Aid of protein/conc. grad to transport across cell membrane

Jejunum absorbs 50%

Ileum absorbs 75%

262
Q

What are the electrolyte changes associated with a proximal duodenal obstruction?

A

hypochloremia, hypokalemic, metabolic alkalosis

not proximal = metabolic acidosis from loss of bicarb

263
Q

What are 2 forms of objective assessment of viability for the SI?

A

Fluroescein = organic dye fluroesencnt under UV light

  • inject 10-15ml/kg IV, assess with Woods lamp

Surface oximetry = compare peripheral

264
Q

What enzymes allow glucose and fructose to enter the intestinal cells?

A

SGLUT1, SGLUT2 (fructose)

265
Q

Arterial supply to the small intestines

A
266
Q

Venous supply to SI

A
267
Q

The mesentery gathers and attaches to the abdominal wall opposite the second lumbar vertebra by a short peritoneal attachment known as the root of the mesentery (1) through which the proximal portion of the cranial mesenteric artery passes.

A
268
Q

The small intestines are structurally composed of four layers: the mucosa, submucosa, muscularis, and serosa. The cells at the base of the villi are dividing, undifferentiated epithelial cells that are primarily involved in fluid secretion. The cells mature and differentiate into immature enterocytes as they pass up the crypt.

A
269
Q

What is the maxium dose of potassium infusion 0.5mEq/kg/hr

A
270
Q

Enzymes involved in digestion?

A

Cholecystokinin = enzymes enter duodenum. Secretin= bicarb from pancreas

Proteins: Trypsin, chymotrypsin, carboypeptidase, aminopepridase

Carbs: amylase, suscrase, lactase

Lipids: lipase, bile acids

271
Q

Key points related to suturing SI

A

Inflammation → collagenase in bowel wall, prolonged lag phase (cat gut causes inflammation and dissolves quickly)

Poor submucoas apposition → healing second intention, worse apposition with 2 layer closure

272
Q

Simple appositional cause inversion/eversion in what percent of simple interrupted and simple continuous closures?

A

Interrupted: 66% eversion

Continuous: 38% inversion, eversion or poor apposition

273
Q

What is the ideal knot tying force for the SI?

A

1.5N

274
Q

What are methods of suture line reinforcement?

A

Omentum - angiogenic, immunogenic, adhesive = sutured better than migrate on own. Can form adhernet sheath that prevents perforation

Jejunal serosal patch

Gallbladder serosal patch - ligate cystic duct, but preseve a.

275
Q

What are 4 ways to deal with lumen disparity?

A
  • uneven suture placement (wider apart on larger side)

Cut at angle

Spatulate

Reduce larger side

276
Q

What is a modefied Gambee stitch?

A

Emerges at the mucosa/submucoas junct = can help mucosal eversion

277
Q

Why is it not recommend to use polypropylene in a continous pattern for closure of an SI R&A?

A

Migrates into intestine and serves as an anchor point for foreign material - 6w to 7m later

278
Q

What are the three stapling techniques for SI R&A?

A

Triangulating end to end anastomosis with TA 30 staplers (3 cartridges - attached pic)

Inverting end to end with EEA stapler

Side to side (function end to end) using GIA

279
Q

End-to-end anastomosis using a triangulation technique and a skin stapler. Place three stay sutures to appose the ends of the intestine and divide the circumference into three equal parts. Apply tension between two sutures. Center the skin stapler between the two segments, then apply staples with gentle pressure approximately 2 to 3 mm apart. Apposed edges of the intestinal wall be slightly evected

A
280
Q

For an inverting end-to-end anastomosis, use an EEA stapler and a transverse stapler. Insert the stapler cartridge into the intestinal lumen through an enterotomy 3 to 4 cm from the transection site. Insert the anvil into the other intestinal end. Tie purse-string sutures securely around the shaft of the stapler. After completing the anastomosis, close the enterotomy with sutures or a transverse stapler

A
281
Q

What are advantages and disadvantages of GIA stapler?

A

Advantages: easy, fast, few cartridges, no lumen compromise, luminal disparty not an issue, length of stapler = stoma size, decrease manipulation of bowel

Disadvantage: cost, need 60mm for GIA (may not be enough room in illium, too big for toy breeds (can use endoscopic linear cutting device), blunting of knife

282
Q

What are complications associated with enteroplication?

A

obstruction, strugulatoin, perforamtion, septic peritonitiis, perforaiton with abcess formation, mid jejunal volvulus

complicaitons usually occur 1m or more post-op, rate of complication higher with enteroplication and rate of recurrence

Experimentally: abdominal discomfort, vomiting diarrhea, decreased appetite, constipation

283
Q

What is the reported incidence of SI dehisence after R&A and after biopsy?

A

7-16%

12%

284
Q

How much fluid can the omentum and peritoneal membrane absorb?

A

3-5% body weight/hour

285
Q

What is the mortalitiy rate post intestinal dehisence?

A

50-85%

286
Q

What are factors that encourage adhesion formation?

A

ischemia, hemorrhage, FB, infection

287
Q

What are factors that can decrease adhesion formation?

A

200ml of peritoneal dialysis solution 3x daily for 4 days after clsoure - likely mechanical removal but may also be fibrinolytic

intraabdominal recombinant tissue plasminogen activator (t-PA) - thrombolytic

288
Q

When does short bowel syndrome occur?

A

Resection of 50% or more of the proximal or distal small bowel (steatorrhea dt removal of distal ileum)

(body wt, cholesterol and albumin lowest after distal resection)

Can occur with 50% but some dogs have 85% resection without a problem

289
Q

What are the causes of short bowel syndorme?

A

Reduced mucosal surface area

gastric and intestinal hypersecretion

bacterial overgrowth

decreased intestinal transit time

290
Q

How fast does contrast agent reach the colon in short bowel syndrome?

A

5-12 min

291
Q

What kind of food should be fed to patients with short bowel syndrome?

A

soluable fiber and glutamine

10-15% fiber: promotes intestinal adaptive changes, modulates motility, increses water resorption, binds excess bile salts (secratory diarrhea)

Fat: delays gastric emptying, calories, stim enterocyte growth

292
Q

What are medications that can be used to treat short bowel syndrome?

A

Loperamide - antidarrhea, increases intestinal tone

Antibiotics - treats intestinal overgrowth - amoxi, tertacycline, metronidazole, tylosin

293
Q

What surgical procedures to treat short bowel syndrome?

A

Construct intestinal vavles

interposition of reversed bowel segment

colonic interposition

reversed electrical pacing

294
Q

What anatomic measurement on radiographs can be used to ID distended small intestine?

A

Measure height body L5

SI:L5 ratio > 1.6 abnormal. >2 very likely FB

295
Q

How can intestinal infarction be diagnosed?

A

mesenteric angiography, contrast MRI (T2), repeated US

focal segments of bowl dilation progress to segmental thickening and loss of normal layer appearence over 24 hr

296
Q

What percent of cats have a linear FB caught around the tonge and what pecent improve with conservative management (i.e. cut the string)?

A

50%

remanant passed in 1-3 days in 47%

297
Q

What percent of linear FB in dogs have peritonitis at the time of sx?

A

40%

298
Q

What is the prognosis for linear FB?

A

Probability of death/peritonitis 2x greater for dogs than cats

Perforations = worse px survival

30% dogs have gross contamination and more than 40% require R&A

299
Q

Define intussusceptum and intssuscepiens

A

Intussusceptum: the part of the intestine that telloscopes in

Intussuscepiens: the lumen the intussusceptum goes into

300
Q

What is the reccurence rate for intususecption and where do they generally recur?

A

6-27% recurrence

recur proximal to previous site

301
Q

Laproscopic treatment iliocolic intusseption - only experimental

A

Laproscopically monitored and manipulated bowel while insuflating rectum with CO2

1 perf, 1 reccur

cannot be done with fibrosis or vascualr collaspse

302
Q

What cuases have beed assocaited with mesenteric vovlulus?

A

lymphoplasmacytic enteritis

ileocolic carcinoma

GI FB

recent GI surgery

blunt abodminal trauma

GDV

EPI

303
Q

What is the signalment for mesenteric volvulus?

A

young male large breed dogs

GSD, English pointers

304
Q

What chemical abnormalities are associated with mesenteric volvulus?

A

hypoproteinemia, hypokalemia, hypoalbuminemia

305
Q

What percent recover after derotation of a mesenteric volvulus?

A

36%

306
Q

What is the sensativity for peroneal penetration?

A

60%

307
Q

What are congenial malforations of the SI?

A

Intestinal diverticula

intestinal duplication

308
Q

Colonic orifaces?

A
309
Q

Colonic blood supply

A

Cr. mesenteric a.

  1. common trunk
    1. Middle colic - desending colon
    2. Right colonic - transverse colon
    3. Illeocololic
  2. Cd pancreaticoduodenal
  3. Jejunal aa.
  4. Ileal aa.

Caudal mesenteric a.

  1. cr. rectal
  2. left coloic (anastomosis with middle colic)

Left colic → caudal mesenteric (middle colic), (ileocolic (right colic and cecal)) → portal v.

310
Q

nervous supply colon

A

PLEXUS MAIN ARTERIAL BRANCHES GROSSLY DISSECTIBLE STRUCTURES SUPPLIED

CONTINUING THE PLEXUS SOURCE

Cranial mesenteric Common colic Cranial mesenteric ganglion Large intestine

Caudal mesenteric Left colic Lumbar splanchnic nn (caudal group) Hypogastric nn (paired) Cranial hemorrhoidal Aortic plexus Distal colon (left)

311
Q

What is the function of the colon?

A

Resovior microbial ecosystem

Resorb: H20, Na, Cl, short chain FA

Secreate: K, HCO3 and mucus

312
Q

Describe electorlyte and water transport in colon

A

Electrical gradient: basolateral Na/K pump, apical brush border K selective channels

Na/k pump (elecrogenic), Na/H 1-3 or Cl/HCO3 (electroneutral

Aquaporins: Colon absorbs 1.5L fluid/d

313
Q

What are the names of the intrinsic plexuses that control motility of the colon?

A

intrinsic plexus:

Myenteric or Auerbach (between longitudinal and circular mm)

submucous or Meissner’s (in submucosa)

314
Q

What do D and M cells do?

A

M cells (microfold):

  • produce proinflammatory cytokines, chemokines
  • move proteins, virus, etc. transepitheliallyto subepithelial lymphoid cells
  • invagination basolateral membrane where memory T and B cells interact and M and D cells interact

D cells:

  • activated migrate to lymph node and prime T helper cells and B cells *humoral immunity
  • also penetrate epithelium and directly sample luminal antigens
315
Q

What are the phases of healing of the colon?

A

Lag phase: 0-3 or 4d - fibrin clot, most likely time for dehisence, platelets initate, then neutrophils d2-3, then monocytes and macrophages

Proliferation phase: 3 or 4 - 14d - fibroblasts proliferate (major by 4d) and clot replaced by collagen, type III collagen 30-40% of granulation tissue (normally 20%), with the remainder being type I. Diven by PDGF, TGF-beta, FGF. Bursting strength almost normal by 10-17d. Angiogenesis.

Maturation phase: 17d onward: collagen reorganize/remodel. Macrophages and fibroblasts decrease, acute thin collagen fibers become thick bundles, amount of type III decreases.

316
Q

What is the collagen content of the submucosal layer?

A

Type I 68%

Type III 20%

Type IV: 12%

317
Q

When does the colon return to 75% of its normal strength?

A

4 months, takes longer than for SI

318
Q

What are factors that negatively effect healing in the colon?

A

hypoprofusion

poor apposition

wound tension

infection

distal obstruction

systemic hypovolemia

blood transfusion (impaired funct or migration of macrophages)

icterus

chemotherapy

immunodeficiency

DM

Zn and Fe deficency

319
Q

When does PaO2 effect collagen synthesis and wound healing?

A

Collagen PaO2 < 40mmHg

Angiogenesis PaO2 < 10mmHg

320
Q

What are methods that may imprve colonic wound healing?

A

Vascularized tissue wraps - omentalplasty (no increase brusting strength, no benefit in people but may help confine leakage, may increase but benefits outway risk), expirmentaly rectus abdominus flaps

Colonic reinforcement - SIS (no association with acute stenosis, adhesions or abcessation)

  • amniotic membrane (experimental, rats)

Cytokines = giving VEGF may increase angiogenesis

321
Q

What are suture less closures of the colon and what are some benefits?

A

Lazers:

  • Na: YAG: low power neodymium-dopedyttrium aluminum garnet : quicker healing with fewer adhesion, initially lower brusting strength
  • gallium arsenide lazer: stronger anastomosis tan sutured

Cyanoacrylates - NOT recommended

Fibrin glue - minimal inflammation and scar, rapid healing (ashesive of thrombin and fibrongen)

322
Q

What have post-op epidurals with bupivicaine been associated with?

A

Intusseption - decrease intersinal paralysis but alters myelectric impulses and propulsion

323
Q

What is a Parker-Kerr pattern?

A

Cushing pattern over a clump, then oversewn with Lembert

324
Q

Where did Bertog suggust as the lanfmark for the colorectal junction and the site to end a subtotal/total colectomy?

A

2cm cr. brim of pelvis, 1cm aborad to the enterence of the cd. mesenteric a.

Subtotal preserves ileocolic valve, 1-2cm distal to ileocolic juntion

325
Q

What is a Furniss clamp?

A

Auto-suturing for purse string placement

326
Q

What are the 2 colostomy techniques reported in dogs?

A

End on colostomy

Loop colostomy

327
Q

What is a paraneoplastic syndrome associated with cecal tumors?

A

Erythrocytosis - leiomyosarcomas (ectopic erythropoiten)

Most common tumors cecum - GIST (/leiomyosarcoma), then adenocarcinoma and sarcoma

MST 681d, 1yr 83%, 2y 62%

328
Q

When is megacolon reversible?

A

If mechanical obstructoin corrected within 6m

329
Q

What are the causes of feline megacolon?

A

Idiopathic 62%

Pelvic stenosis: 23%

Neurologic disorder: 6%

Manx 5%

330
Q

What is the theroy behind megacolon?

A

Generalized dysfunction of longitudinal and circular smooth mm. seconday to disturbance in activation of smooth mm. myofilaments - no histologically sp. abnormality

331
Q

What is the signalment of megacolon in cats?

A

Middle aged male cats

332
Q

What is the radiographic basis of megacolon?

A

Normal colon: diameter = length of L2

Colon > 1.5x the length of L7 = megacolon

333
Q

What is the medical management of megacolon in cats?

A

Stool softeners

high-fiber diet

periodic enemas

cisapride - benzmide class: prokinetic causes release of acetylcholine from enteric nervous system which stimulates contraction fo snooth m. in descending colon

334
Q

What do phosphate enemas cause in cats?

A

rapid dehydration, hypocalcemia, hypophospatemia and death

335
Q

How to discern primary from seconday megacolon in cats

A
336
Q

How to manage idopathic megacolon

A
337
Q

how to manage seconday megacolon

A
338
Q

How does lactulose work?

A

disaccharide not hydrolyzable by mammals

Bacteria digest into organic acids → increase osmotic pressure in lumen of colon → retain water

339
Q

What are surgical treatments for megacolon?

A

Coloplasty with partial colectomy = recurrence

Subtotal or total colectomy

  • ileocolic orifice acts as sphincter = prevent reflux, removal may cause SIBO or increased severity/incidence of diarrhea
  • end to end, end to side, and side to side colocolostomy or entercolostomy
340
Q

How long does it take for normal enteric motility to re-establish?

A

8 weeks

Some cats do not adapt (increase vilus height, entercyte number/density) and have chronic diarrhea

Recurrence of constipation is ucommon but one study had 45% recurrnece rate. Stricutre rare.

341
Q

What are concurrent or previous diseases associated with coloinc and cecocolic volvulus?

A

Medium to large, young dogs

previous intussusception and EPI or GDV with gastropexy

342
Q

What are common colonic tumors in cats and dogs?

A

Dogs: Adenocarcinoma, LSA, stromal tumors, extramedullary plasmacytoma

Cats: LSA, adenocarcinoma, MCT, neuroendcrine tumors

343
Q

What are the MST for common colonic tumors in dogs and cats?

A

MST Dogs: ACA - 6-22m, GIST- 37m, Leiomyosarcoma 7.8m

MST Cats: ACA - subtotal colecotmy 138d, R&A 68d. LSA 97d, MCT 199d

mets at the time of sx in cats: ACA 80%, LSA 75%, MCT 75%

344
Q

What is the difference between type 1 and type 2 colonic duplication?

A

Type1 : limited to colon and rectum

Type 2: associated with other congenital abnormalities (urogenital duplicaitons, veterbral colum abnormalities

Subclassified: spherical noncommunicating, tubular noncommunicatong, tubular comminucating

345
Q

What is the vascular supply to rectum/anus?

A

Vaculature: intrapelvic

  • Cranial rectal a. (majority)
  • Internal iliac → Internal pudenal a
    • Middle rectal
    • Caudal rectal
  • Cats = intraplevic adequately supplied by middle and cd. Rectal (NOT dogs, need cr. Rectal)
346
Q

General anatomy of rectum

A
  • Retroperitoneal portion: lacks serosa – implications for healing
  • Anal canal – 1cm length
    • Columbar zone
    • Intermediate zone = anocutaneous line
    • Cutaneous zones
      • Internal zone
        • Anal glands
        • Anal sacs - ivaginations
      • External zone
        • Circumanal glands (perianal, hepatoid)
    • Anal glands (tubular swear glands): columnar and intermediate zones
      • Glycoproteins (alpha-l-furctose) = viscoelastic properties mucus
347
Q

Describe the ventral approach to the rectum

A
  • Pubic symphysiotomy
  • Pubic or pubic and ischial osteotomy increses exposure
  • Ideally at least 2cm normal tissue should be removed on either side
348
Q

Describe dorsal approach to the rectum

A
  • U shaped incision between anus and tail (extend to tubur ischium)
  • Rectococcygeus mm, dorsal rectum and sphinctes are visible
  • Rectoccygeus mm transected at attachement on coccygeal vertebra
  • Blunt dissect between the levator ani and sphintermm. And levator ani transected if needed
349
Q

Describe rectal pull though

A
  • Rectal pull through, transanal pull through
    • If incison made at anal-cutaneous junct = incontence and removal of anal sacs, start 1.5cm internally to avoid this
350
Q

Describe Lateral approach

A
  • Resection of a rectal diverticulum, rectocutaneous fistula, repair laceration of rectum
  • Curvilinear perianal incision – tail base to ischium
  • Dissect between external anal sphincter and levator ani
351
Q

What causes incontinence in colorectal surgery?

A
  • Pelvic plexus at peritoneal reflection disrupted
  • Anal sphincter removed
  • Removal distal 1.5cm may (even if anal sphincter persevered) = incontinence
    • Resection of 6cm (with peritoneal reflextion) through dorsal approach = incontinence
      • Transection alone or resection 4cm defecated normally
    • Resection of more than 6cm with reflextion and maintaining distal 1.5cm = no incontinence
352
Q

Describe the types of atresia ani?

A
  • Aresia Ani
    • Type 1: congenital stenosis
    • Type 2: persistence anal membrane, inperforate anus with blind pouch
    • Type 3: Like 2 but blind end further cranially
    • Type 4: caudal rectum/anus normal but cranially has blind pouch
353
Q

How does a rectovaginal or urethrorectal fistula form?

A

failure of the urorectal septum to separate the cloaca into anterior urethrovesical segment and posterior rectal segement

Possibley more common in poodles

Commonly present with atresia ani

354
Q

What is a anogenital cleft?

A
  • Have cloaca, ventral aspect anus incomplete and forms dorasal part of cleft
  • Males often have hypospadias
355
Q

What are methods of treatment of rectal prolapse?

A
  • Reduce prolapse/edema: saline, lubricants, 50% dextrose, liver yeast cell derivative, systemic furosemide
    • Apply purse string 3-5d (time to tx underlying cause)
    • Dicyclomine anticholinergic-antispasmatic
    • Retention enema with hydrocortisone or mesalamine
  • Rectal resection and anastomosis – place tube and cut full thickness (see Fig 94-12).
  • Multiple recurrence = colopexy
    • No difference between incisional colopexy and scarifcation with 2 rows of 5 or 6 simple interrupted sutures
356
Q

What hormone is associated with perianal adenomas?

A

Androgens (testosterone)

Look for cushings disease in females

Adenocarcinoma is not hormone dependent

357
Q

What factors are assocaited with prognosis for perianal adenocarcinoma?

A
  • Stage only factor for survival and DFI
  • >5cm and mets increased death 11x and 45x respectively
  • recurrence increased with >5cm and invasion of tissue
  • Nuclei size correlated with ln mets and survival
358
Q

What is the metastatic rate of perianal adenocarcinoma at diagnosis?

A
  • 14.6% mets at dx – ln, lungs, liver, bone, kidney
359
Q

What is a paraneoplastic syndrome seen with adenomatous polyps?

A

leukocytosis

hypocholesterolemia and hypoalbuminemia also common

360
Q

What are treatment options for benign rectal tumors?

A
  • Mucosal eversion
  • Electrosurgery/ligation – small lesions
  • Cyrotherpay – applied to base prevent regrowth
  • Transanal endoscopic biopsy = more diffuse leasions: 38% cured, 20% palliated, 50% poor (15% death due to perf)
361
Q

Surigcal treatment options for perianal fistula

A
  • Excision sinus +/- anoplasty (if around entire anus), cryosurgery, sx debride and chemical cauterization (not recommended due to cytotoxicity), high tail amputation, deroofing and fulguration, laser excision
362
Q

Perineal hernia types

A
  • Caudal perineal hernia: btwn levator ani, internal/external anal sphincters
  • Dorsally: coccygeus and levator ani
  • Ventrally: ischiourethralis, bulbocavernosis and ischiocavernosis mm.
  • Latearlly coccygeus, sacrotuberous lig. (sciatic perineal hernia)
363
Q

Muscles and improtant structures for perineal hernia

A

Muscles:

  • Levator ani: attach 7th cd vertebra, external anal sphincter
    • Iliocaudalis
    • Pubocaudalis – inserts perineal body
  • Coccygeus: originates spine of ishium, attach transvers process 2-5th lumber vertebra
  • External anal sphincter: 3rd cd vertebra and levator ani
  • Internal obturator
  • Sacrotuberous lig: ischiatic tuberosity to sacrum and 1st cd vertebra
  • Ischiorectal fossa: laterally levator ani/coccygeus, dorsal/lat superficial gluteal, dorsal external anal sphincter and ventral internal obturator, constrictor vulae female, retractor penis make
364
Q

Bounderies perineum?

A

3rd cd. Vertebra, sacrotuberous lig. And ischial arch

365
Q

Breeds with perineal hernia

A

intact older males 83-93%

  • Breeds: Pekingese, Boston, corgis, boxers, poodles, bouviers, old English, collies, doxies, kelpies, GSD
366
Q

Causes perineal hernia

A
  • Association with non-traumatic inguinal hernias
  • Rectal abnormalies: result not cause
    • 100% rectal deviation, 40% rectal dilatation
  • Androgens
    • Risk recurrence 2.7x greater if not castrated
    • Castration reduces recurrenc rate 23-43%
    • Possibly low quanity of androgen rectors in diaphragm mm., but upregulation not seen post castration in dogs with perineal hernia unlike normal dogs
  • Gender related anatomic differences
    • Larger/broader levator ani mm with longer rectal attachment, larger sacrotuberous lig., peritoneal cavity ends more cranially, breed exceptions (greyhounds/bboxers)
  • Relaxin = higher expression relaxin receptors, no diff conc.
    • Leakage of cystic prostatic fluid with relaxin may predispose to pelvic and inguinal hernias
  • Prostatic disease
    • 25-59% concurrent prostatic disease
    • Neutering may not effect recurrence when prostate normal
  • Neurogenic atrophy
    • Poss dt traction of sacral plexus during straining
    • High incidence spontaneous potentials on electromyographic recordings of pelvic diaphragm mm.
367
Q

Perineal anatomy

A
  • Levator ani: attach 7th cd vertebra, external anal sphincter
    • Iliocaudalis
    • Pubocaudalis – inserts perineal body
  • Coccygeus: originates spine of ishium, attach transvers process 2-5th lumber vertebra
  • External anal sphincter: 3rd cd vertebra and levator ani
  • Internal obturator
  • Sacrotuberous lig: ischiatic tuberosity to sacrum and 1st cd vertebra
  • Ischiorectal fossa: laterally levator ani/coccygeus, dorsal/lat superficial gluteal, dorsal external anal sphincter and ventral internal obturator, constrictor vulae female, retractor penis make

Blood supply:

  • Internal pudendal: courses over internal obturator m.
368
Q

What percent of perineal hernias are unilateral

A
  • Unilateral 47-66% R>L (59-84%)
369
Q

What percent perinal hernias have bladder retroflexion?

A
  • Bladder retroflexion 20-29%
370
Q

Surgical preparation of the perineal area. Incision A, traditional perineal herniorrhaphy; incision B, superficial gluteal transposition; 1, purse-string suture in the anus; 2, iliac crest; 3, greater trochanter of the femur; and 4, ischial tuberosity. The incision for the internal obturator muscle transposition should extend 2 to 3 cm ventral to the ischial tuberosity.

A
371
Q

What are surgical options for perineal hernia?

A

Surgical options:

  • Herniorrhaphy
  • Internal Obtrator Muscle Transposition
    • Do not go past caudal edge of foramen to avoid obturator n. damage
  • Superfical gluteal m. transposition
    • Tendon isolated below biceps m. and cut at insertion on the trochanter tertius - reflected and sutures to external AS
    • Must preserve n. and blood supply (still attached to sacrum, sacrotuberous lig. and gluteal fascia
    • Can include part of fascia lata
    • Modefication: tendon of insertion transected and roated 45 degrees – sutured to internal obturator, sacrotuberous, external anal sphincter
  • Combination of internal obturator and supficial gluteal (internal on bottom and sutured to tail, superficial to ischial fascia)
  • Semitendinosus m. transposition
    • Good as salvage or if ventral defect
    • Recommend contralateral m. for unilateral defect
    • Do not injure caudal gluteal a. = transect midbody/stifle
  • Prosthetic implants
    • Mesh: 92% success rate
      • Complication: suture sinsuses (resolved once suture removed)
    • PSIS
      • As strong as internal obturator m. trans. And normal diaphram
    • Porcine dermal collagen
      • Serosanguinous dc 33%, success rate 59%
    • Fascia Lata
      • Very good outcomes, lameness associated with donor site most common complication
  • Pexy
    • Colopexy
    • Cystopexy
      • Has been used to treat dysuria secondary to caudally displaced bladd
    • Vasopexy
      • Castration with ductus vigated separt from vasculature
      • Tunnel transverse abdominal m at level of apex empty bladder
      • Each passed through tunnel and sutured to self
      • Doesn’t prevent bladder retroflexion
    • Laparoscopic vasopexy: 66% free CS at 8m
    • Complications pexy: tenesmus most common, fever, constipation
    • Complications staged: urine dibbling (37,17% permanent), tenesmus (44%, 10% permant), wound complicaitons (17%), recurrence 10%
372
Q

How do you treat unusal perineal hernias?

A

Surgical options:

  • Herniorrhaphy
  • Internal Obtrator Muscle Transposition
    • Do not go past caudal edge of foramen to avoid obturator n. damage
  • Superfical gluteal m. transposition
    • Tendon isolated below biceps m. and cut at insertion on the trochanter tertius - reflected and sutures to external AS
    • Must preserve n. and blood supply (still attached to sacrum, sacrotuberous lig. and gluteal fascia
    • Can include part of fascia lata
    • Modefication: tendon of insertion transected and roated 45 degrees – sutured to internal obturator, sacrotuberous, external anal sphincter
  • Combination of internal obturator and supficial gluteal (internal on bottom and sutured to tail, superficial to ischial fascia)
  • Semitendinosus m. transposition
    • Good as salvage or if ventral defect
    • Recommend contralateral m. for unilateral defect
    • Do not injure caudal gluteal a. = transect midbody/stifle
  • Prosthetic implants
    • Mesh: 92% success rate
      • Complication: suture sinsuses (resolved once suture removed)
    • PSIS
      • As strong as internal obturator m. trans. And normal diaphram
    • Porcine dermal collagen
      • Serosanguinous dc 33%, success rate 59%
    • Fascia Lata
      • Very good outcomes, lameness associated with donor site most common complication
  • Pexy
    • Colopexy
    • Cystopexy
      • Has been used to treat dysuria secondary to caudally displaced bladd
    • Vasopexy
      • Castration with ductus vigated separt from vasculature
      • Tunnel transverse abdominal m at level of apex empty bladder
      • Each passed through tunnel and sutured to self
      • Doesn’t prevent bladder retroflexion
    • Laparoscopic vasopexy: 66% free CS at 8m
    • Complications pexy: tenesmus most common, fever, constipation
    • Complications staged: urine dibbling (37,17% permanent), tenesmus (44%, 10% permant), wound complicaitons (17%), recurrence 10%
373
Q

What are complicaitons of perineal hernias?

A
  • Traditional: 28-61%
  • Internal: 19-45%
  • Gluteal: 15-58%
  • Incisional infection 6.4-45%
  • Other complications: rectal prolapse, urinary abnormalities, rectocutaneous fistula, anal sac fistulation, flatulence, pain on defecation
  • Incontinence <15%
  • Sciatic n. injury <5%
    • Use caudolateral approach to the hip
  • Bladder atony 15-29% with entrapment, dribbing can occur with or without (37%, 17% irreversible)
    • Mortality rate of 30% in one report
  • Tensmus:
    • Inflammation, severe rectal dilatation, tension on bilateral repair, suture rectal wall.
    • Incidence 44-50% with colopexy
    • Rectal prolapse 2-13%
  • Recurrence
    • 0-70%, traditional 10-48, internal 0-46, gluteal 36%
    • Factors related: surgeon experience (10 vs 70%), pervious repairs (83vs43%), type of suture, local tissue strength, amount of tension, ongoing predisposing factors, neutered vs intact
    • Sacculation associated with lack ventral diaphragm
      • 8/31 swelling, 11/31rectal sacculation, 9/31 lack ventral, 7 lack dorsal and ventral.
374
Q

uture placement for traditional herniorrhaphy (caudolateral view). 1, external anal sphincter; 2, coccygeal muscle; 3, superficial gluteal muscle; 4, ischial tuberosity; 5, internal obturator muscle elevated from ischial table; and 6, retractor penis muscle.

A
375
Q

emitendinosus muscle transposition for repair of recurrent bilateral perineal hernias in a Yorkshire terrier (also pictured in Figure 94-30). Previous bilateral internal obturator transpositions and subsequent unilateral prosthetic mesh placement had failed. A, The circumference of the semitendinosus muscle is isolated, taking care to avoid injury to the caudal gluteal artery and vein (visible at the tip of the electrocautery unit). B, The muscle is transected distal to the midbody and freed with gentle dissection as it is reflected dorsally. Lateral tendinous attachments can be incised to improve mobility. C, The muscle has been sutured to external anal sphincter medially, levator ani and coccygeus remnants dorsally, and superficial gluteal muscle laterally. D, Final appearance 1 day after surgery. The dog maintained a rounded appearance of the dorsal perineal region because of obesity and thickness of the transposed muscles; however, the hernias did not reoccur.

A
376
Q

Anatomic arrangement of the liver lobes and extrahepatic biliary tract. A, Diaphragmatic aspect of the liver. B, Visceral aspect of the liver. C, Liver lobes, gallbladder, and hepatic ducts, visceral aspect

A
377
Q

Ligaments of the liver?

A

Coronary lig. = liver to diaphram

  • 2 right triangular ligaments: larger = lateral, smaller = medial
  • Left side trigangular lig

Hepatorenal lig = caudate to kidney

Lesser omentum (surrounds papillary process)

  • hepatogastic lig.

- hepatoduodenal lig.

- faliciform lig.

378
Q

How long can the pringle manuver be performed?

A

20 min before liver necrosis

379
Q

Describe blood supply to liver

A

Hepatic a = 20% blood, 50% oxygen

  • 2-5 branches: R lat (caudate, R lat), R middle (R med, dorsal quadrate, L med), Left (L lat, L med, quadrate)
  • Cystic a.

Portal V. = 80% blood, 50% oxygen

  • confluence cr. and cd. mesenteric v. at left pancreas
  • additional tribitaries: splenic, gastroduodenal (not in cats)
  • Right main br (caudate, R lat)
  • Left main br - L lat, L med, quadrate
      • Central br (R med, pap)

Cats: 3 main branches: Right, central, left

6-8 hepatic vv. into cuadal vena cava - most cr. near diaphram

380
Q

Describe the flow of bile.

A
  1. Canaliculi
    1. interlobular ducts
      1. Lobar ducts (inside parachyma) = Hepatic ducts (2-8 ducts)
        1. Common bile duct (where 1st hepatic joins cystic)
          1. Sphincter of Oddi (CBD enters duodenum)
          2. Duodenum (major duodenal papilla)
381
Q

What are the differences between dogs and cats related to the major and minor duodenal papilla?

A
  1. Ducts (pancreatic and CBD) separte in dogs and have sphincter of Oddi, but combined in cats
  2. Minor duodenal papilla (acessory pancreatic duct) - major duct for pancreas in dogs, but absent in 80% cats
    - damage to the Major papilla can cause EPI in cats.
382
Q

What are the Vit K dependent coag facors?

A

2, 7, 9, 10

383
Q

Liver functions?

A

Synthesis/clearence plasma proteins

Maintain carbohydrate/lipid metabolism

Synthesis coag factors/anticoagulents

Carboxylation Vit K dependent coag fators

Modyfy immune fuction

Production bile and synthesis hormones (gastrin)

Storage VIt, fat glycogen, metals

Clearence toxic metabolites

Maintatin glucose conc

Synthesis cholesterol

384
Q

What coag factors not produced by liver?

A

factor 8 and von wilbrands

385
Q

What clotting factors does the liver produce/

A

plasminogen, antithrombin 3, alpa2-macroglobulin, alpa2-antiplasmin

386
Q

What do Kuffer cells do?

A

Hepatic macrophages distributed througout hepatic sinusoids

Primary reticuloendothelial celll

endotoxemia, sepsis, drug sens may result if reticuloendothelial system compromised

387
Q

What is bile?

A

bile acids

bilirubin

cholesteral

phospholipids

water

bicarb

ions

388
Q

How is bilirubin produced?

A

80% hemoglobin breakdown

20% metabolism of proteins (myoglobin)

389
Q

Describe life cycle of bilirubin/bile?

A

Bilirubin bound to albumin → transported to liver

In hepatocyte bilirubin conjugated to glycine/taurine (dogs) or taurine (cats)

Conjugated biliribin and bile acids in gallbladder

Cholecystolinin release from intestinal mucosa → GB contract, sphincter relax

—- Bile salts emulsify fats (aid digest and absorpotion), bind endotoxin, prevent absorption into portal circulation

Bilirubin → urobilinogen (by bacteria) → urobilin or stercobilin (90% excreated, 10% resorbed)

—-small amount urobilin excreated by kidneys, stercobilin give feces brown color

390
Q

How does the liver funciton in protein metabolism?

A

20% total body protein production

100%albumin, also alpha, beta, gama globulins and coag proteins

391
Q

How is cholesterol synthesized and fat stored in liver?

A

Cholesterol: chylomicrons and lipoproteins

Stores fat as trigylcerides from FA

392
Q

How much liver can be removed in a normal dog?

A

65-70%, but not 84%

  • 28% survived 7d after 80% heptatecotmy
  • death due to portal hypertension

Concurrent side-side portal caval shunt improved survival to 57%

393
Q

What portal pressure decreases survial and liver regeneration post heptatectomy?

A

16mmHg

394
Q

How much does liver volume increase after portal embolization in dogs?

A

25-33%

Aids in contralateral liver hypertrophy prior to resection.

Afer 70% heptaectomy - compensated hypertrophy as early as 6d may take 6-10w

Can resect upto 95% liver if done as repeated partial heptectomy

395
Q

What factors contribute to liver regeneration?

A

cytokines (IL6, TNF alpha)

Growth factors (Hepatic GF, epidermal GF, TGF beta)

Vasoregulators (NO, PGE2)

hormones (insulin, estrogen)

396
Q

What factors impede regeneration?

A

Billary obstruction → decrease blood flow

DM

Pancratectomy

nonhepatic splanchnic eviscereation

total nonhepaticc evisceration

malnutrition

male/old age

397
Q

What is the hepatic arterial buffer response?

A

Increase in hepatic arterial perfusion seconaday to lack of washout of senosince (vasodilator) via portal circulation (aka disruption in portal profusion)

398
Q

What happens with acute ligation of the CBD?

A

increased bilirubin and dilated CBD in 24-48hr

dilation lobar and interlobular ducts at days 4-6

hypotension, decreased myocardial contractility, ARF, GI hemorrhage, coags, delayed healing

  • absence bile salts = bacteria overgrowth/endotoxin absorption = acute tubular necrosis, incaresed acid secreation, gastric ischemia, decrease fibroplasia, andiogensis
399
Q

What percent of choleliths are radiopaque?

A

50% dogs (calcium bilirubinate), 80% cats (calcium carbonate)

400
Q

What is the correlation between FNA and histopath for liver aspirates?

A

30-48% dogs, 51% cats

401
Q

What is contracst enhanced harmonic ultrsongraphy?

A

Detects harmonic signal produced by IV injection of gas microrbubbles to evalute perfusion patterns of different organs

402
Q

What is the noramal diameter of the CBD?

A

3-4mm

403
Q

How gallbladder emptying be tested?

A

Give IV sincalide (synthetic cholecystokinin)

normal empty 40% GB in 1hr

abnormal <20%

404
Q

Methods of EHBO?

A
  • *US**
  • *Hepatobiliary scinthigraphy -** IV tech99 - isolates in bilary tree, EHBO if not in SI by 3hr
  • doesn’t differentiate functional from mechanical obstruction or site

CT (=US for splenic metastatic HSA)

MRI - 100%sens, 94% specific benign vs malignant hepatic lesions

Endoscopic retrograde cholangiopancrreatography

- also allows stent placement

405
Q

What procoagulents and anticoagulents does the liver produce?

A

Procoagulent: coag factors, fibrinogen, vit K, thrombopoetin

Anticoagulent: protein C, proteinS

Removes activated coag factors and fibrinogen degredation products

406
Q

What percent of dogs with liver disease have at least one coag abnormality?

A

57%

407
Q

What percent of dogs/cats with hepatobilliary disease had a positive culture?

A

dog: 5%, 50% single organism
cat: 14%, 83% single organism

Enteric most common: Clostridum, e coli, entercoccus, bacteroides)

Billiary cultue more often positive (30% vs 7%)

408
Q

What are materials used for hemostasis of the liver?

A

gelatin sponge - smaller but present at 45d with fibrin layer

ozidized regenerated cellulose - dissolved at 45d, no reaction

cyanoacrylate glue

fibrin glue

409
Q

What are methods for hepatic blood flow occulsion?

A

Inflow occulsion = Pringle maneuver

Hepatic a. ligation

  • need abx (gangerous necrosis), cholecystectomy, lobar aa ideally
  • 95% blood supply to tumor vs 20% liver paranchyma

Total inflow/outflow occulsion = Cr. and Cd. VC and inflow occlusion

  • w pringle gastroduodenal v, retrograde arterial flow through gastroduodenal a. and back bleeding through hepatic vv.
410
Q

What is the accuracy, complication rate and px factors of percutaneous liver biopsy?

A

43-83% accurate

Complications: 22% minor (>10% HCT no intervention), 6% major (transfusion, death)

Complication factors: thrombocytopenia <80K, prolonged PT/PTT

Not reccomended in cats with EHBO = vagogenic shock

411
Q

What are methods for liver lobe biopsy?

A

Fracture/guillotine

Punch

Ultrasonically activated scapel (aka harmonic scapel)

Laproscopic liver biopsy - biopsy forceps or loop ligature

412
Q

How does surgical ligation compare to stapler for hepatic lobe removal?

A

Dissection/ligation: slower, less complete, associated with more mircoscopic hemorrhage, necrosis and inflammaiton

413
Q

How can you deal with expected excessive portal hypertension from liver lobectomy?

A

Ipsilateral portal v. embolization

create portocaval shunt

414
Q

What percent of the liver do the right, middle and left segments make up?

A

Right lateral/caudate = 28%

Right medial/quadrate = 28%

Left medial/latearl = 44%

415
Q

What are percutaneous tumor ablation techniques?

A

Radiofrequency

Microwave

laser thermal

cryoablation

ethanol ablation

416
Q

What percent of dogs and cats have a postive culture for EHBO, mucocele and bile peritonitis?

A

EHBO dogs: 17-39%, cats: 30-50%

Mucocele: 23-60%

bile peritonitis: 58-61%

417
Q

What are surgical procedures of extrahepatic billary tract?

A

Cholecystocentesis

Cholecystoduodenostomy

Choledochoduodenostomy

Billary stenting

Cholcutostomy tube

Cholecystectomy

CHoledochal catheterizaiton

418
Q

What are indications for laproscopic cholecystectomy?

A

GB mucocele, cholelithiasis or cholecystitis not associated with EHBO, GB rupture,

419
Q

What were the outcomes in dogs and cats treated with choledochal stenting?

A

Dogs = no reobstruction

Cats = 2/7 reobstruct within one week

420
Q

What are common bacteria reported for hepatic abcesses? And what are treatment options?

A

E.coli, staph, enterococcus, klebsiella, clostridium

Medical alone, US drainage, sx resection

Percutaneous US and alcholization

421
Q

What is the prognosis for hepatic abcsesses?

A

Dogs 50% euthanize, however those treated responded well

Cats: 79% euthanized, 3/4 favorable response to treatment - 2 cases concurrent HCC, none of the cases in dogs had malignacy

422
Q

What is the most common liver lobe to have a torsion?

A

Left lateral

Good px if treated quickly, associated with abscess, septic peritonitis, hernia, tumor, hepatitis, GDV - recommend pexy

423
Q

What is the underlying lesion of GB mucocele and what breed is predisposed?

A

Cause: cystic mucosal hyperplasia - hypersecreation of mucus - can cause EHBO or GB rupture

Shetland sheep dogs

424
Q

What endocrinopathies are associated with GB mucocele?

A

Cushings = 29x higher, 21% of dogs with cushing’s have mucoele (vs. 2%)

Hypothyroidism = 3x higher, 14% of dogs with hypothyroidism have mucocele

425
Q

What is the sensativity of US for GB rupture?

A

85.7%

426
Q

What percent of GB mucoceles cultured positive and what type of bacteria?

A

Aerobes 9-75%

Anaerobes 0-25%

Enterococcus and E coli most common

427
Q

What percent of cases have a GB rupture and what percent have concurrent EHBO?

A

23-60%

concurrent EHBO 30%

428
Q

What percent of dogs with choleliths have positive cultures?

A

70% aerobic

55% anaerobic

some bacteria produce beta-glucoronidase = deconjugates soluble bilirubin = clcium bilirubinate

429
Q

What percent hepatocellular tumors are adenomas?

A

30%,

hepatocellular carcinoma most common 50-70% of non-hemopoietic neoplasms

430
Q

What percent of HCA had mets?

A

61% are massive and have mets in 36%

  • 67% left lobe (20-80% with leasions other lobes), 12-20% central or right

30%/10% are nodular/diffuse and have mets in 93%

mets ln (39%), lungs (38%), peritoneum (18%), also anywhere else

431
Q

What is the px for massive HCA?

A

MST 1460d with removal, 270d with medical management

Periop mortality 5%

Incomplete margins ~10%, not associated with recurrence

Right side tumors poorer px

432
Q

List the tributaries to the portal v. (caudal to cr)

A

Cr. Mesenteric vessels

Cd mesenteric vessels

Splenic

Gastroduodenal

433
Q

Hepatic veins

A
434
Q

Describe the embyronic deveolopment of the liver

A

vitelline vessels = hepatic sinusoids, cr. right becomes cd. vena cava in liver, right and left cd segements anastomos to become portal v.

umbilical v = hepatic sinusoids

cardinal = anastomse with vitelline to make cd vena cava, right suprecardinal = azygos, left supracardinal = hemiazygos

Embryology of liver development. 1, Sinus venosus; 2, superior cardinal vein; 3, inferior cardinal vein; 4, left common cardinal vein. 5, right umbilical vein; 6, liver; 7, anastomosis between the left and right omphalomesenteric vein; 8, right umbilical vein (prehepatic); 9, left umbilical vein; 10, right omphalomesenteric vein; 11, umbilical vein (unpaired); 12, inferior vena cava; 13, ductus venosus; 14, portal vein; and 15, splenic vein.

435
Q

What congenital abnormality is associated with left sided intrahepatic shunts?

A

Patent ductus venosus

Usually functional closure 2-6 d (wolfhounds 65% 4d, 23% 6d, all 9d)

structural closure 3 weeks

436
Q

What causes ductus venosus contraction?

A

Cytochrome p450 and thromboxane = contract

PGF1 alpha and PGE2 = relax

Steroids → inhibit phospholipase A2 → decrease PG → increase acitivity alpha adrenoreceptors = contract

437
Q

What percentage of dogs have a single intrahepatic or extrahepatic shunt?

A

Intra = 25-33% (larger portion of blood shunting, CS eariler)

Extra = 75-66%

438
Q

What percent have aquired shunts, where are they usually located and what are the common causes?

A

20%

Portal tributary to renal v. or CVC, less common gonadal or internal thoracic

Cirrhosis, PVH with portal hypertension, Hepatic arteriovenous malformations

439
Q

What is portal vein hypoplasia (PVH) without portal hypertension characterized by?

A

AKA microvascular dysplasia, 58% dogs, 87% cats also have macroscopic PSS

  • sm. intrahepatic portal vessels
  • portal endothelial hyperplasia
  • portal v. dilatation
  • random juvenile intralobular blood vessesl
  • central venous hypertrophy
440
Q

Types of PSS

A

Types of portosystemic shunts in dogs and cats. A, Portal vein to caudal vena cava. B, Portal vein to azygos vein. C, Left gastric vein to caudal vena cava. D, Splenic vein to caudal vena cava. E, Left gastric, cranial mesenteric, caudal mesenteric, or gastroduodenal vein to caudal vena cava. F, Combinations of the above.

441
Q

Toxins that cause hepatic encephalopathy and their MOAs.

A

Ammonia Increases brain tryptophan and glutamine; decreases ATP availability; increases neuronal and cellular excitability; increases glycolysis; can cause brain edema; decreases microsomal Na+,K+-ATPase in the brain

Aromatic amino acids Decrease DOPA neurotransmitter synthesis; alter neuroreceptors; increase production of false neurotransmitters

Bile acids Membranocytolytic effects alter cell membrane permeability; make the blood-brain barrier more permeable to other hepatic encephalopathic toxins; impair cellular metabolism because of cytotoxicity

Decreased α-ketoglutaramate Diversion from Krebs cycle for ammonia detoxification; decreased ATP availability

Endogenous benzodiazepines Neural inhibition through hyperpolarization of neuronal membrane

False neurotransmitters Impair norepinephrine action

Tyrosine → Octopamine Impair norepinephrine action

Phenylalanine → Phenylethylamine Synergistic with ammonia and SCFA

Methionine → Mercaptans Decreases ammonia detoxification in the brain urea cycle; gastrointestinal tract derived (fetor hepaticus breath odor in hepatic encephalopathy); decreases microsomal Na+,K+-ATPase

GABA Neural inhibition by hyperpolarizing neuronal membrane; increases blood-brain barrier permeability to GABA

Glutamine Alters blood-brain barrier amino acid transport

Phenol (from phenylalanine and tyrosine) Synergistic with other toxins; decreases cellular enzymes; neurotoxic and hepatotoxic

SCFAs Decrease microsomal Na+,K+-ATPase in brain; uncouple oxidative phosphorylation; impair oxygen utilization; displace tryptophan from albumin, increasing free tryptophan

Tryptophan Directly neurotoxic; increases serotonin through neuroinhibition

442
Q

What metabolic derangements are associated with hepatic encephalopathy?

A

hypoglycemia, dehydration, hypokalemia, alkalemia

443
Q

What is the signalment for extra and intrahepatic PSS?

A

Intra = irish wolfhouns (left division, genetic assoc), Aussies (right division), retrievers

Extra = sm breed (yorkie, havanese, maltese, dandie dinmont, pugs, schnauzers) = OR 20x

  • yorkies OR 36x

Cats: DSH, siamese, persians, himalayans, burmese

PVH-MVD = carins

PVH hypertesion = Dobbies (27%), usually <4y, >10kg

444
Q

Why are PSS dogs PU/PD?

A

low BUN conc = poor medulary gradient

INcreased renal blood flow

Increased ACTH secretion

Psycogenic HE

445
Q

What percent AV malformations have abdominal effusion?

A

75%

446
Q

What are common secondary problems with inta hepatic PSS that are less common with extrahepatic?

A

GI signs, especially gastic ulceration (30% with intrahepatic = GI protectents)

IBD

447
Q

What percent of shunts have urinary calculi and why?

A

30% = ammonium urate

decresed urea production

increased renal ammonia

decrased uric acid metabolism

448
Q

What are clinical signs more commonly seen in cats with PSS?

A

Ptyalism 75%

copper colored eyes

also cyrptorchid (30%), 50% dogs are cyrptorchid

449
Q

What common clin path findings associated with PSS?

A

Microcytosis - defective Fe transport

Leukocytosis

Mild increases in liver enzymes (ALP>ALT)

Low albumin (50%), Low BUN (70%), low cholesterol, low glucose

Decreased Cre

UA: low USG (>50%), ammonium biurate crystalluria (26-57%, dog, 16-42% cat), hyperammonuria, proteinuria (100% severe glomerulopathy)

450
Q

What can effect bile acids testing?

A

timing GB contraction

rate intestinal transport

decrease BA deconjugation

Rate/efficency absorption in ileum

Portal blood flow

functionality of epatocyte uptake and canalicular transport

451
Q

What cause false + and false - for bile acids testing?

A

False +: inappropriate sample timing, other hepatobillary disease, cholestasis, steriods, anticonvulsant therapy, trachal collapse, seizures, GI disease

False - : Prolonged transport, lack GB contraction, inadequate food uptake, delayed gastric emptying, malabsorption/digestion

452
Q

What percent have abnormal ammonia conc? How can this be tested?

A

62-88% with PSS

Basal, sens increased to 91% when 6hr post-prandial

  • basal affected by prolonged fasting, protein restriction, lactulose (not affected with ATT)

Ammonia tolerance test (ammonium chloride), test 30min post giving (sample must be tested in 20min), sens =95-100%

  • hyperammonemia = methylmalonic acidemia, urea cycle enzyme deficientcy (cats, deficient ornithine transcarbamylase), urethral obstruction
453
Q

What coag factors are produced in the liver?

A

factors I (fibrinogen), II (prothrombin), V, VII, VIII (vascular endothelium), IX, X, XI, XIII, as well as protein C,protein S and antithrombin.

454
Q

How are PT and PTT affected by liver disease?

A

65-80% factor loss = prolonged PT or PTT

Chronic disease - increased PTT (common with PSS, factor deficiencies common (2,5,10) and extrinsic (7))
Acute = increased PTT and PT

Coag status returns to normal 6w postop if no persistent shunting

455
Q

What is protein C?

A

VitK dependent serine protease

Activated by thrombin = anti-thrombotic, anti-inflammatory, antiapoptotic

Normal dogs = 70% activity or greater

Differentiates 95% MVD (>70%) from 88% shunt (<70%), doesn’t differ MVD from normal

456
Q

What are common histopath findings with dogs with PSS, MVD, AV malformations, etc?

A

Increased/hypertrophied: Bile duct proliferation/hyperplasia (hx worse px), Arteriolar proligeration/duplicaiton, Smooth m. hypertrophy, Increased lymphatics around central v., Ito and Kupffer cell hypertrophy

Hypoplasia/atrophy: Hypoplasia of intrahepatic portal tributaries, Hepatocellular atrophy

Lipidosis/cytoplasmic vaculolar changes (lipogranulomas) - 55% dogs

necrosis (hx worse px)

fibrosis (hx worse px)

None associated with px for intra or extra hepatic shunts

457
Q

Radiographic findings of PSS?

A

Microhepatica (60-100% dogs, 50% cats), bilateral renomegaly

Not necessarily seen with portal v. hypoplasia

458
Q

What is the sens and specif of diagnosing extra and intra hepatic shunts on US?

A

Extrahepatic: Sens 75-95%, Spec 67-100%

Intrahepatic: Sens 95-100%

Distinciton intra vs extra: 92%

459
Q

What flow changes occur with various shunts on US? What is normal flow?

A

Normal portal flow 15cm/sec

AV malformations = hepatofugal

Extrahepatic PSS = hepatopedal flow, increased/variable velocity in 53% (92% with intrahepatic)

Extrahepatic decrased portal v:arota size

460
Q

What is the 1/2 life of techntium pertechnetate?

A

6hr

461
Q

What are the methods for scintigraphic ID of shunts and what are the limitations?

A

Dx: arrives sooner and in higher conc. than expected to heart, PSS shunt fract >60-80%, 52% cats

Transcolonic: (99mTcPertechnetate) shunt fraction <15% normal, false + if injected too caudal, heart visible 8-14sec, higer dose = isolate for 16-24hr

Transsplemic: (99mTcO4-) lower shunt fraction, 100% sens/spec for PSS, in heart 2-4 sec, uptake poor with portal hypertension, cleared 30 min

Increased shunt fraction with: PSS, aquired PSS, and AV malformations. Doesn’t distinguish intra from extra or intra, single from multiple and MVD from normal…at least reliably for the first 2.

Transsplenic scintigraphy. A, Extrahepatic portocaval shunt in a Labrador retriever. Blood flow from the spleen enters the heart at its caudodorsal aspect. B, Portoazygos shunt in a Yorkshire terrier. Blood flow from the spleen enters the heart at its craniodorsal aspect. C, Multiple acquired shunts in a Chihuahua. Blood flow travels caudally from the spleen before entering the caudal vena cava

462
Q

What methods for diagnosis of a PSS?

A

US

Scintigraphy (transcolonic, transsplenic)

CT angiogram (ideally duel phase, also trassplenic CT portography)

MR angiogram (spec 97%, sens 67-79% w/o gadolinium)

Portovenography - cr. to 13th rib = intrahepatic, sens = 85% dorsal, 91% right lat, 100% left lat)

Percutanous US guided splenic portovenography

Pretrograde tranjugular portography

Cr. mesenteric arteriography (via femoral - alot of contrast, hard to interpet)

463
Q

How do you medically manage severe hepatic encephalopathy?

A

Warm water enema

Oral/rectal lactulose

Antibiotics → decrease in urease producing bacteria (metro, ampi, neo)

Anticonvuslsants (benzos + maintance)

Mannitol (HE = cerebral edema people)

Lactulose (per os or high enema) - acidifiy lumen and binds ammonia, decreases bacteria numbers, also decreases fecal transit time

If needed whole blood (packed rbcs have ammonia)

Diet = milk/veg protein, 20% dogs, 30% cats

Acid receptor blocker if intrahepatic (omeprazole life long)

Ascites = diuertics (spironolactone), drugs that decrease connective tissue (pred, colchicine, D-penicillamine)

Neutraceuticals: SAMe, ursidiol, Vit E, Milk thistle

464
Q

What is the px with medical managements liver shunts?

A

MST 10m, decreased TP, ALT, ALP (no other changes)

65% intra and 33% extra euthanized

50% med management survived long term, 88% sx survived long term - age no effect on survival

MVD: 92% longterm survival

HPV with hypertension - 40% long term survival but should be consisder favorable

465
Q

Side effects of overdose of Iohexol from portoveinography?

A

hypotension, arrhythmias, cardac arrest, renal failure

dose 240mg I/ml 2-5ml/kg (not exceed 1200mg/kg)

466
Q

Additional interpretation of portovenogram

A

Cats: more arborixation after shunt ligation = less likely postop neuro comp and better response to sx

Dogs: absence arborization prior to ligation = greater occurence postop complications

  • more portal branching, better able to withstand complete ligation
  • response to sx not correlated with preligation portal development
467
Q

How much of the ameroid constrictor diameter reduces?

A

Reduces by 32%, use ring larger than vessel (hydroscopic)

Gas sterilized = do not use within 12-24 hours

468
Q

How do you determine the degree of shunt attenuation?

A

86% require partial ligation, (70% regain normal liver funct)

Portal hypertension: pallor, cyanosis of intestines, increased GI peristalsis, cyanosis/edema of pancreas, incrased mesenteric vasular pulsations.

Postligation pressure: max 17-24cmH20 (12.6-17.6mmHg), change P of 10cmH20 (7.35mmHg), max ecrease in CVP of 1cm H20 (0.74mmHg)

Decrease arterial P max 5mmHg (<15%)

Shunt ligated to the point where shunt flow hepatopedal and cr. portal v. hepatopedal to avoid aquired shunts

469
Q

Intravascular hepatic shunt - left division

A

Venous dilatation at junct. left hepatic v. patent ductus venosus and left phrenic v = ampulla

Usually ligate shunt (bwteen papillary process and L lat lobe before enters L hepatic v. ) OR heptatic v.

If shunt can’t be ID then left portal v.

The left hepatic vein (LHV) enters the left side of the caudal vena cava (CVC) just cranial to the diaphragm. The central hepatic vein termination is indicated with an asterisk. B, The space between the CVC and LHV is gradually enlarged with right-angle forceps, which are advanced in a dorsolateral position

470
Q

Intravascular hepatic shunt - right division

In dogs, the portal vein (PV) bifurcates approximately 1 cm distal to the termination of the gastroduodenal vein (GDV). The left hepatic vein (asterisk) is much smaller in this dog with a right intrahepatic portosystemic shunt

A

Ligate portal v. (see above) or intravascular technique

If can’t directly disect, then can do indirect suture passage

Indirect suture passage for ligation of a right intrahepatic portocaval shunt. In a dog with a right-sided shunt, the portal vein would be much larger than the left

471
Q

Intravascular approach Portal venotomy

A

Need total inflow occlusion = pre/post hepatic cd. vena cava, thoracic aorta, and portal v./hepatic a. through epiploic foramen

  • mean arterial P = 30mmHg, mean CVC pressure = 25mmHg

Intravascular repair of an intrahepatic portocaval shunt through a portal venotomy. A, The portal vein is exposed and the dilated prehepatic segment (star) is identified. B, After inflow occlusion, a venotomy is performed. The edges of the portal venotomy are retracted with stay sutures (arrows), and the shunt ostium is identified. C, A suture (5-0 prolene) is passed across the shunt ostium and though pledgets. D, The venotomy is closed with a simple continuous pattern, and inflow occlusion is released. The attenuating suture is subsequently tightened. CVC, Caudal vena cava; LL, left lateral; PV, portal vein; QU, quadrate; R, rumel; RHV, right hepatic vein; RL, right lateral; RM, right medial; S, shunt.

472
Q

Intravascular approach transcaval approach

A

Intravascular repair of an intrahepatic portocaval shunt, diaphragmatic view. The suture is passed through extraluminal and intraluminal Dacron pledgets in a mattress pattern

473
Q

How are platelets and clotting factors affected by acute ligation?

A

Plt. count decreases 27%

Factors 2,5,7,9,10,11, fibrinogen decrease 10-16%

PT increases 7%

PTT no change

2-14% develop acute hypertension

474
Q

What percent have seizures?

A

Dogs: 3-18%

Cats 8-22%

upto 80 hr post-op

475
Q

What are potential causes of post-op seizures in PSS?

A

Decreases in endogenous inhbiory CNS benzos agonist levels

Imbalance in excitatory and inhibitory NT

Concurrent neurologic disease

Hyponatermia = seizures/coma when <120meq/L, increase slowly (1meq/h) or fatal cerbral edema and potine myelinosis

476
Q

What are the periop mortality rates and long term outcome for EH PSS

A

Periop mortality: suture 2-32%, AC, 7%, cellophane 6-9%

Longterm: good 78-94% (any technique), 35% euthanized (mean 43m) after partial lig (recurrence), only 11% normal at 1yr with partial ligation.

477
Q

Mortality rate and long term outcome IH shunts?

A

Mortaliity: suture 6-23%, AC 0-9%, Cellophane 27%

Good long term: 70-89% AC, 76-100% suture, 50% cellophane

Proability of survial without recurrence: 60% 1yr, 55% 2-4yr

Hydraulic occulder: immediate survival 100%, 30% require revision, 80% long term survival. complications recurrence, sinus tract development

478
Q

What factors have been associated with short term outcome for PSS

A

IH: >10kg more favorable, Higher TP/albulmin = better survival, Increased BUN = decreased short term survival (not long term)

Breeds not associated with PSS more likely to have unusual/inoperable PSS

Acute ligation:

  • Non-encephalopathic dogs can tolerate complete occlusion more often
  • Greater liver size likely to tolerate acute ligation
479
Q

Factors associated with long term outcome for PSS in dogs.

A

POOR: anemia, leukocytosis/neutrophilia, albumin decrease by 1 = odds continued shuting increased 3.76x (EH/AC), greater increase in portal pressure

GOOD: TP>4 (IH), Every albumin increase 1 = unsucessful odds decreased 0.4 (EH/AC), better survial EH than IH one paper,

480
Q

Factors that have not effect on outcome in PSS for dogs.

A

Age at surgery

Body weight

Pre-op neuro signs

Pre-op bile acids (EH)

Pre-op histopathology

Location of coil embolization

481
Q

What is the outcome in cats with PSS?

A

Periop mortality: 0-4% (AC, suture), 0-23% cellophane

Post-op complications: upto 75%

  • neuro most common, seizure 8-28%, central blindness up to 44% (persisting neuro signs not associate with siezures, shunt location, degree attentuation, age

Of surviving cats, good outcome 56-75% (suture), 33-75 (AC), cellophane 80%

Persistent shunting = excellent outcome

482
Q

Where are hepatic AV malformations located?

A

Right or central divisional lobes

Usually 1, 20% 2

Portal v. normal in size.

Treat by lobe resection, periop survival 75-91%, longterm 38-57%, 75% still need medical management

Complications: portal hypertension, systemic hypotension, braycardia, portal or mesenteric v. thrombus

483
Q

What is the Branham reflex?

A

reflex bradycarida with closure of hepatic AV fistula

484
Q

reveiw page on interventional rad for venous liver malformations

A
485
Q

What are the 4 poplypeptide secreting islet cell types and what do they secreate?

A

alpha → glucagon

beta → insulin

delta → somatostatin

Fcells/PP cells → pancreatic polypeptide

486
Q

What is the blood supply to the pancreas?

A

Celiac

→ splenic

→ hepatic → cranial pancreaticoduodenal

Cr. mesenteric → cd pancreaticoduodenal

487
Q

What is the innervation to the pancreas?

A

vessels: celiac and cr. mesenteric plexus

acinar and islet cells: cholinergic nerurons that synapse with vagal fibers

pancreatic juice secration: stimulated by parasympathetic, inhibited by sympathetic

488
Q

Describe pancreatic ducts

A

Dog: 68% single duct from each limb

  • accessory pancreatic duct (minor duodenal papilla) = duct of santorini (most important dogs)
  • pancreatic duct (major duodenal papilla) = duct of wirsung

Cats: 80% only pancreatic duct, fuses with bile duct

489
Q

What does insulin and glucagon do?

A

Insulin: stimulates anabolic reactions (carbs, lipids, protein, nucleic acids), decrease blood conc of glucose, fatty acids, amino acids. Promote intracellular conversion into glycogen, triglycerides, protein. Controls glucose efflux from extracellular space into insulin-sens cells (adipocytes, monoctyes, hepatocytes)

Glucogon: controls glucose inflex from hepatocytes, secreased in response to hypoglycemia, mobilizes energy stores by increasing glycogenolysis, gluconeogensis, lipolysis

490
Q

What are zymogens secreaeted from the pancreas?

A

Inactive zymogens: typsinogen, chymotrypsinogen, proelastases, procarboypeptidses, prophospholipases. Activated by enteropeptidase (duodenum)

Enzymes: lipase (fats), amylase (starches)

Inorganic components (ductal cells): water, na, K, Cl, bicarb, intrinsic factor (aborption B12)

491
Q

What are the 3 mechanisms that prevent autodigestion?

A

1) enzymes stored and secreated as inactive proenzymes/zymogens
2) Segregated storage of zymogens (packed as membrane bound granules in endoplasmic retriculum)
3) acinar cells synthesize panreatic secretory trypsin inhibitor (stored with enzymes to prevent premature activation)

492
Q

How do nervous and hormonal mechanisms cause pancreatic secreation?

A

smell food → vagal stimulation

movement food into duodenum

→ secretin → bicrab rich fluid (second phase 8-11hr postprandial bicarb rich)

→ cholecystikinin → digestive enzymes (1-2hr post prandial)

493
Q

Bile duct anatomy near major duodenal papilla

A
494
Q

What are pancreatic biopsy techniques?

A

Distal right limb pancreas

Tru-cut, wedge, suture fracture, blunt dissection and ligation, laproscopic

Suture vs. blunt = no diff CS, amylas or lipase. Suture increase inflammation on histo

Complications: swelling, pyrexia, abdominal pain, vomiting, Adhesion (common in cats)

495
Q

How much of the pancreas can be removed?

A

75-90% as long as ducts intact

large regenerative capacity (5% left increased in weight by 50% in 6 w)

potentially due to insulin like GF-1 (max levels 3 days postop)

496
Q

What are tests for EPI and pancreatitis?

A

EPI = TLI (typsin like immunoreactivity) = sens and spec EPI

PLI = panraetic lipase immunoreactivity (82% sens and specific canine, feline 100% mod/severe, 54% sensitive for mild)

497
Q

What is the prognosis for surgical managment of pancreatitis?

A

overall survial 63%

EHBO with cholecystoenterostomy = 80%

necrosectomy 64%

pancreatic abcess 40%

498
Q

For pancreatic abcess, what is the postive culture rate and what is the prognosis when treated with surgery as recommend.

A

In vet patients pancreatic abcess are often sterile

Positve pancreatic culture ranged 0-27% (positive abdominal culture 58% in one study)

Prognosis: 14-55% survival, another study 40%

62% surival rate with omentalization

499
Q

Where do the majority of pancreatic pseudocyst occur?

A

Left limb pancreas

500
Q

How to treat pancreatic peusdocyst?

A

may shrink on own (monitor if <4cm)

External drainage with US

Internal drainage: cystoduodenostomy, cystojejunostomy, cystogastrostomy, omentalization

Complete excision

>75% sucess/survival rate

501
Q

What lab finding is potentially indicative of pancreatic carcinoma?

A

lipase > 25x upper limit

Paraneoplastic alopecia noted in cats

502
Q

What percent of insulinomas are carcinomas?

A

60%

503
Q

What can insulinomas produce besides insulin?

A

glucagon, somatostatin, pancreatic polypeptide, gastrin

504
Q

What is the metastatic rate of insulinoma?

A

50%

lymph nodes and liver most common

505
Q

What side effect can occur with prolonged exposure to glucose?

A

neuronal demyelination and axonal degeneration

ataxia and weakness may not resolve

506
Q

How to diagnose insulinoma?

A

US: pancreatic mass 56%, mets 19%

CT: increased diagnosis, however false positive results for mets screening common 71%

  • duel phase diagnosed 3/3 dogs

Scintigraphy and single photon emission CT with radiolabled somatostatin = to other methods like US

507
Q

What are methods of treatment of post-op or recurrent hypoglycemia

A

streptozocin: nitrosura anitbiotic - kills beta cells = normoglycemia 163 d
diazoxide: benzothiadiazine derivative = inhibits insulin secreation, stimulates gluconeogensis, stim glycolgenolysis, inhibits glucose use

Octreotide: long acting synthetic somatostatin analogue - insulin synthesis

Prednisone

508
Q

What is the prognosis for insulinoma?

A

surgery = more likely to become normocgylcemic, stay that way and survive longer

Dogs with not met: 14m euglycemic, 18m MST

Dogs with mets: 2m euglycemic, 7-9m MST

Dogs with sx and treated with pred when recurrence = MST 1316 vs 785d with only surgery

509
Q

Where do gastrinomas arise from?

A

Pancreas most common, then duodenum, peripancreatic ln, and mesentary

70% metastatic disease (ln, liver)

GI ulceration 80%

Dx with elevated serum gastrin conc while fasting or abdominal explore, too small for imaging

Px: 1w to 18m, isolated case 26m

510
Q

How to place pharyngostomy tube

A

Nerve damage, hemorrahge, if not caudal dorsal enough interfers with epiglotis = aspiration, cough, knking, dyspnea, etc.

Indictor for oral disease

511
Q

Methods for esophagostomy tube placement

A

manual treanesophageal advancement

needle=assited percutaneous placement

tube assisted percutaneous placement

Eld percutaneous feeding tube placement

Esophageal feeding tube applicator

512
Q

Percutaneous tube esophagostomy. A, Stiff guide tube placed in midesophagus. B, Catheter passed through the skin and into the tube. C, Forceps placed in the catheter hub and advanced into the guide tube. D, Forceps pulls large feeding tube out through skin. E, The tip of a large feeding tube is sutured to tip of esophagostomy tube. F, The large feeding tube pulls esophagostomy tube into the mouth. A stylet is placed in the esophagostomy tube. G, The esophagostomy tube is withdrawn until it can be redirected distally. H, The tip of the esophagostomy tube is advanced to the distal esophagus.

A
513
Q

Percutaneous esophagostomy using an Eld applicator. A, The Eld applicator is placed in the esophagus, and the trocar is advanced through a small skin incision. B, The feeding tube is sutured to the eyelet of the Eld trocar. C, After the feeding tube is pulled into the oral cavity, a stylet helps to redirect the feeding tube into the esophagus

A
514
Q

What is this?

A

Feeding tube applicator

515
Q

What are methods of gastrostomy tube placement?

A

Surgical - mushroom tipped catheters, low profile (midline or left paracostal approach)

Percutnaeous endoscopic gastrostomy tube

non-endoscopic percutaneous tube placement (semi rigid orogastric tube, metal tube, Eld applicator)

516
Q

Placement of percutaneous endoscopic gastrostomy tube. A, An over-the-needle catheter is placed through the skin and into the air-distended stomach. B, A suture threaded through the catheter is grasped by endoscopic forceps and pulled out through the mouth (C). D, An over-the-needle catheter is threaded onto the suture, which is tied to the gastrostomy tube (E) and subsequently pulled into the stomach and out the gastric and body wall. F–G, The tube is pulled through the skin and secured with a flange. The mushroom-tipped end of the gastrostomy tube should press snugly against the gastric mucosa.

A
517
Q

Tube-assisted percutaneous nonendoscopic gastrostomy. The angled tube is inserted through the esophagus into the stomach at a level caudal to the last rib. Extending the patient’s head over the end of the table facilitates palpation of the tube through the abdominal wall. A, The flared end of the tube in the stomach is pressed against the left abdominal wall, displacing other intra-abdominal organs. B, A needle is passed through the skin into the flared end of the tube, and a strand of heavy suture or wire is passed through the needle into the stomach and advanced out of the mouth. The remainder of the placement is the same as that for a percutaneous endoscopic gastrostomy tube.

A
518
Q

Percutaneous nonendoscopic gastrostomy with an Eld device. A, The device consists of a cannula with a handle and a trocar that is passed through the cannula after it is properly positioned. B, The device is advanced through the esophagus and into the stomach so it is beyond the last rib. The trocar is pushed through the cannula until the tip exits the skin, and a suture is tied onto the tip (inset). C, The trocar is retracted into the cannula (inset), and the device and attached suture are withdrawn through the animal’s mouth. The remainder of the placement is the same as that for a percutaneous endoscopic gastrostomy tube.

A
519
Q

Low-profile gastrostomy device (arrowhead). Pressure on the obturator (solid arrow) elongates the mushroom tip for placement through the gastrocutaneous fistula (open arrow). The mushroom tip regains its conformation when the obturator is removed

A
520
Q

Enterostomy tube placement. A, An antimesenteric incision is made through serosa and muscularis, and the feeding tube is advanced through a mucosal perforation at the aboral end of the incision. B, Serosa and muscularis are sutured with an appositional pattern over the tube, and a purse-string or mattress suture is placed around the tube at its orad seromuscular exit site.

A
521
Q

Needle-assisted enterostomy. A, A needle is passed obliquely through the center of a purse-string suture, creating a subserosal tunnel in the antimesenteric intestinal wall. B, A feeding tube is passed through the needle and advanced 20 to 30 cm aborally. The needle is removed, and the purse string is tied

A
522
Q

What are enterostomy tube options?

A

Standard

Needle assisted techniqque for tubes without catheter adaptors

Needle assisted technique for tubes with catheter adaptors

Gastroenterostomy tube (via PEG or open)

Duodenostomy (limited approach with L block)

Low profile enterostomy tube

523
Q

What is another name for a mushroom tip Gtube?

A

Pezzar tip

524
Q

What is the daily water requirements for dogs/cats

A

50-100ml/kg/day

525
Q

What is the most that can be fed?

A

22-30ml/kg

526
Q

What is refeeding syndrome?

A

Decreased potassium, phosphorus and magnesium

Causes weakness, fluid retention, arrththmias, dyspnea, vomiting, diarrhea, illeus, renal dysfunction, tetany

527
Q

Examples of commercially available clamps designed for use with linear external skeletal fixation systems. A, Kirschner-Ehmer clamp; single and double clamps (IMEX Veterinary Inc., Longview, TX). B, SK clamp; single and double (IMEX Veterinary Inc.). C, Securos external skeletal fixator clamp (Securos, Sturbridge, MA). D, Titan external skeletal clamp (Securos). Black arrow, position for transfixation pin; white arrow, position for connecting bar

A
528
Q

How does adding a unilateral plate agumentation steel connecting plate or 2nd steel connecting bar add to the stiffness of a type 1a fixator?

A

Steel plate = 4.5x increase axial stiffnes and med/lat bending, 2x increased cr/cd bending and stiffness

Double steel connecting bar = 80% stiffer in axial and 170% stiffer in med/lat beneing compared to external plate.

= stiffness of IIb or 50% IIa

529
Q

Which is more important, bar diameter or pin number?

A

larger diameter bar to increase stiffness negated when 2 or more full pins used

530
Q

What factos improve stiffness type 1 fixators?

A

stonger frame

hybrid design

Tie-ins

threaded pins

531
Q

At what point will pin number not increase stiffness?

A

>4 per segment

532
Q

What size pins should be used and at what spacing for ESF?

A

no greater than 20-30% bone diameter = stress riser

Evenly spaced, no closer than 3x pin diameter or 1/2 bone diameter from joint/fracture

533
Q

What can be done to decrease bone resorption around the pins?

A

reduce pin-bone interface stress

smooth pins at 70 degrees to long axis

position bar closer to the bone = stiffer construct

Pin stiffness porportinal to the pin length^3 (shorter is stiffer)

No chuck (wobbles), power drill <150rpm

60 degree pin offset = 4-5x stiffness in 1a (acylics)

534
Q

What are the advantages of circular ESF?

A

1- increased stiffness in bending/shear and decreased stiffness in axial compression

  1. small fragmenrs 1-1.5cm
  2. adjustable after placement
535
Q

What are the 15 principles of ESF application?

A
  1. Aseptic technique
  2. Proper locaiton for pin insertion
  3. Select most suitable ESF
  4. Auxillary fixation when indicated
  5. Maintain stabilization and reduction when applying frame
  6. Insert pins without damaging soft tissues
  7. proper pin insertion technique
  8. Engage both corticies
  9. insert smooth pins and neg. profile pins at 70 degree angle
  10. Insert all pins in same plane when using bar
  11. Even distribution - optimize mechanical stability
  12. 3-4 pins in each fragment
  13. Optimal size implants
  14. Optimal distance between clamps and skin
  15. Cancellous graft in sig cortical defects
536
Q

How does the use of ESF effect surgery time and healing time for comminuted tibia fractures?

A

Decreased surgery time 45%

Decreased healing time 27%

537
Q

What is the incidence of mal/non-union in small breed dogs treated with exernal coaptation for radial fractures?

A

83%

538
Q

What are the guidelines for external coaptation?

A

Reduction = at least 50% contact of cotical fracture fragments

Proper alignment

Neural standing angle

immobilize joints above and below

539
Q

What is this?

A

Robinson sling

Other wierd slings = schroeder thomas

540
Q

What are grades of sprains?

A

Grade 1 = overstretch ligament

Grade 2 = partial tear

Grade 3 = complete tear

541
Q

What are types of orthoses?

A

Non-ridgid, semi-ridgid, Rigid

Static vs. Dynamic

Stifle braces: prophylactic, rehabilitative, funcitonal

Contracture/assist type braces

542
Q

What are the types of non-unions?

A

Viable = mechanical issue (motion, fracture gap), biologically OK

  • Hypertrophic
  • Moderately hypertrophic
  • Oligotrophic - some biologic failure as well (loose implant at fracture- prevent bone proliferation and vascularization.

Non-viable = biologically inactive

  • Dystrophic - compromised vasculature/non-viable bone 1 or both sides
  • Necrotic - infected dead bone = sequestrum
  • Defect - gap too large and filled with non-bone (fibrous or muscle)
  • Atrophic- result of above types, host removes bone but doesn’t replace
543
Q

What are less conventional methods to deal with delayed/non-unions?

A

Extracorporeal shock wave - hypertrophic but not atrophic

Pulse electromagnetic field

Low intensity pulsed US

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