96.Hepatic Vascular abN

Question 1

percentage of congenital PSS that are single extrahepatic

Answer 1

66-75% of congenital PSS = single extra hepatic25-33% of congenital PSS = intrahepaticportocaval is most common singe EHPSS

Question 2

causes of acquired PSS

Answer 2

20%older animalsmultiple, tortuous, extrahepaticnear kidneys, gonads, or internal thoracic veins1. cirrhosis/ hepatic fibrosis2. portal vein hypoplasia WITH PH (congenital noncirrhotic PH)–dobies over rep3. hepatic AV malformations

Question 3

other name for PVH without PH

Answer 3

portal vein hypoplasia without portal hypertension=microvascular dysplasia (MVD)bc portal vein hypoplasia can occur with or without portal hypertension

Question 4

percentage of dogs/cats with congenital PSS and MVD

Answer 4

PSS with MVD60% dogs90% cats

Question 5

hepatic encephalopathy occurs when what percentage of the liver is dysfunctional

Answer 5

HE occurs with 70% liver function is lost

Question 6

most important neurotoxin for HE

Answer 6

Ammonia (produced by GI flora)increases brain tryptophan (neurotoxic) and glutaminedecreases ATP increases neuronal excitability (excitotoxic)increases NMDA receptors w glutamatebrain edema, seizures

Question 7

MOA of benzodiazipines and GABA for causing HE

Answer 7

neural inhibition through hyper polarization of neuronal membranecoma, stupor, depression

Question 8

MOA bile acids for causing HE

Answer 8

membranocytolytic effects alter cell membrane permeability making BBB more permeable to other substances

Question 9

causes of coagulopathy in liver failure

Answer 9

decreased factor synthesisincreased factor utilizationincreased fibrinolysissynthesis of anti coagulants decreased platelet function and numbervit K deficiencyincreased production of anticoagulants(TEG may suggest these patients are hyper coagulable)

Question 10

odds ratio of Yorkshire Terriers for occurrence of congenital PSS

Answer 10

35.9 times greater than all other at risk breeds combined for occurrence of congenital PSS

Question 11

other toy breeds affected with congenital PSS

Answer 11

suspect hereditary–yorkshire–maltese–cairn

Question 12

breeds overrepresented with intrahepatic PSS

Answer 12

larger breeds–irish wolfhounds–retrievers–australian cattle dogs–australian shepherd

Question 13

type of intrahepatic PSS in irish wolfhounds

Answer 13

left divisional intrahepatic PSShereditary in irish wolfhounds

Question 14

type of intrahepatic PSS in australian shepherds

Answer 14

right divisional intrahepatic PSSoverrepresented in australian shepherds

Question 15

MOA of PU/PD in PSS dogs

Answer 15

extremely common PU/PDMOA–medullary washout of BUN–increased renal blood flow–increased ACTH–psychogenic PD from HE

Question 16

abdominal effusion in hepatic arteriovenous malformations in dogs

Answer 16

75%also seen with multiple acquired PSSand more common in intrahepatic vs extra hepatic PSSlikely cause–hypoalb (decr production liver, PLE from GI ulcers or IBD +/- lymphangiectasia)

Question 17

preoperative GI hemorrhage reported in PSS patients

Answer 17

30% intrahepatic PSS—treat w gastroprotectants prepuncommon in extrahepatic PSS

Question 18

ptyalism reported in cats as clinical sign of PSS

Answer 18

75%

Question 19

causes of lower urinary tract signs in PSS patients

Answer 19

decreased ureaincreased renal ammonia excretiondecreased uric acid metabolismammonium urate calculi 30%+/- secondary bacT infection

Question 20

clinicopathologic findings for hepatic vascular anomaly patients

Answer 20

microcytosis, normochromic nonregenerative anemia (iron sequestration)target cells–dogs; pokiolocytes–catsthrombocytopenialeukocytosis (associated with poor px)hypoalb, hypogly, decreased BUN, hypocholesterolmoderate incr liver enzymesbile acids incrUA–decr USG, crystalluria

Question 21

protein C and ddx btwn PSS vs MVD

Answer 21

Protein C = antiinflm, antithrombotic, antiapoptotic (vit K dependent)PSS 88% patients had levels < 70%PVH–MVD 95% patients had levels > 70%cannot ddx normal vs PVH-MVD

Question 22

flow of hepatic AV malformations vs extrahepatic PSS on doppler US

Answer 22

hepatic AV malformations–hepatofugalextrahepatic PSS–hepatopedal

Question 23

diagnostic imaging for hepatic vascular anomalies

Answer 23

survey radsab USscintigraphy–transcolonic< transsplenic (technetium pertechnetate)CT angiographyCT transplenic portographyMR angiographyPorto(jejuno or spleno) venography–intra-operative, fluoro, 2-4 ml/kg iohexolother: percutanous US transsplenic venography, retrograde transjugular portography, cranial mesenteric angiography via femoral artery

Question 24

normal scintigraphy shunt fractions

Answer 24

transcolonic shunt fraction < 15% normaltranssplenic shunt fraction &laquo_space;15% normalmost congenital PSS >60-80% SFincreased in dogs with single congenital IHPSS/EHPSS, multiple acquired shunt, hepatic AV malformations

Question 25

disadvantages of scintigraphy

Answer 25

cannot ddx intra vs extra hepatic PSScannot ddx normal vs PVH-MVD dogscannot ddx single vs multiple

Question 26

dose for intra-operative portovenography

Answer 26

2-4 ml/kg iohexol (sterile, water soluble 240-360 mg I/ mL)jejunal or splenic vein catheterizationfluorocranial to 13th T IHPSScaudal to 13th T EHPSSlife threatening hemorrhage if splenic injection at AV malformations present

Question 27

MOA and dose lactulose

Answer 27

0.5-1.0 ml/kg PO q6-8hr to effect5-10 ml/kg warm water enemapromotes acidification which traps luminal ammonium and decreases colonic bacT #also osmotic effect, reduces transit time

Question 28

diuretic of choice to treat ascites from portal hypertension

Answer 28

spironolactone bc of potassium sparing effectsascites from decreased oncotic pressure however can be treated with colloidal therapy

Question 29

epiploic foramen

Answer 29

dorsally---caudal vena cavaventrally--portal vein caudally--celiac artery/hepatic artery

Question 30

most common area to find multiple acquired PSS

Answer 30

1. near right kidney2. within intestines

Question 31

normal portal pressures

Answer 31

measured through jejunal, splenic, or portal vnormal 8-13 cm H20 (6-10 mm Hg)patients with PSS have lower PP

Question 32

ameroid constrictor material

Answer 32

inner casein--hygroscopic substance absorbs fluid decreasing inner diameter by 32%outter stainless steel

Question 33

suture ligation of PSS

Answer 33

non absorbable synthetic monofilament2-0 silkpolpropylene to decrease risk of shunt recanalization

Question 34

signs of portal hypertension

Answer 34

pallor or cyanosis of intestinesincreased intestinal peristalsiscyanosis/edema of pancreasincreased mesenteric pulsations

Question 35

what percentage of dogs require partial shunt attenuation

Answer 35

86%

Question 36

where is the ductus venous visible

Answer 36

ductus venosus is visible btwn left lateral lobe and papillary process of the caudate lobe before it enters the left hepatic veinmost dogs with left sided IHPSS have a patent ductus venousfunctional closure 2-6 daysstructure closure 3 weeks

Question 37

what are portocaval windows

Answer 37

when portal vein and cava vascular walls fuse

Question 38

list post operative complications PSS

Answer 38

hypoglycemia (44%)hemorrhage/anemiaportal hypertension (2-14% acute)hypothermiaseizures/HE (18% dog 22% cat day 5)recurrence of clinical signs

Question 39

propofol CRI for PSS post op seizures

Answer 39

0.1-1.0 mg/kg/min

Question 40

mortality rates for surgically treated EHPSS

Answer 40

2-32% suture ligation7% ameroid6-9% cellophane

Question 41

mortality rates for surgically treated IHPSS

Answer 41

6-24% suture ligation9% ameroid27% cellophane(higher rates with intrahepatic attenuation)

Question 42

portal vein tributaries

Answer 42

FROM CAUDAL TO CRANIAL--cranial mesenteric vein (largest)--caudal mesenteric vein--splenic vein--gastroduodenal vein (absent in cats)

Question 43

three types of classifications of liver vascular disease

Answer 43

1. congenital PSS2. primary hypoplasia of portal vein (abN hepatic blood flow or portal hypertension)3. disturbances in portal outflow

Question 44

treatment for acute severe HE

Answer 44

--warm water enema--oral or rectal lactulose--dextrose administration--fix metabolic acidosis with IVF--antibiotics metro, neomycin, amoxiclav)--anticonvulsants

Question 45

Greenhalgh et al 2010 JAVMA medical mgmt vs surgery for treatment of PSS and survival

Answer 45

long term survival in med tx alone 50%long term survival with surgery 90%age did not have a significant effect on survival time

Question 46

prognosis for PVH-MVD (no portal hypertension)

Answer 46

excellent 90% long term survival

Question 47

prognosis for PVH with portal hypertension

Answer 47

poor 40% long term survival

Question 48

list 6 reasons for persistent post operative clinical signs

Answer 48

---ligated/device on wrong vessel--more than one shunt--placed too distal and missed a proximal branch--device didn't occlude--acquired shunts develop--PVH-MVD in addition to PSS

Question 49

list 6 methods to correct PSS

Answer 49

--ameroid--cellophane--silk ligation--hydraulic occluder--amplatzer intravascular plug--thrombogenic coil--cardio cyanoacrylate

Question 50

methods to find IHPSS intraoperatively

Answer 50

---compression of parenchyma may lead to increase PP at site of IHPSS--intraop mesenteric/splenic portography--portal or transsplenic catheterization--intraoperative doppler ultrasonography

Question 51

methods for IHPSS dissection/occlusion

Answer 51

intravascular--require temporary occlusion of portal vein/caudal vena cava; transcaval or portal venotomy approachesextravascular approach

Question 52

T/Fin dogs undergoing ameroid occlusion for EHPSS, preop neuro status did not have affect on outcome

Answer 52

TRUEMehl et al 2005 JAVMA

Question 53

complications in cats postoperative shunt occlusion

Answer 53

75%mostly neurologic dysfunction--seizures (30%) and blind in (45%)central blindness may resolve within 2 month

Question 54

treatment for hepatic AV malformations

Answer 54

most often seen in Right and central divisionlobectomy/resection

Question 55

T/Fage at the time of surgery for shunt occlusion had no effect on outcome

Answer 55

true

Question 56

factors that may be negative predictors of outcome

Answer 56

NOT age at surgery, NOT preop neuro status, NOT post op bile acids, NOT liver biopsymaybe:leukocytosis, neutrophiliaanemiahypoalbuminemialarge breed dogs (have recurrence)