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TnJ > 96.Hepatic Vascular abN > Flashcards

96.Hepatic Vascular abN Flashcards

1
Q

percentage of congenital PSS that are single extrahepatic

A

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

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2
Q

causes of acquired PSS

A

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

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3
Q

other name for PVH without PH

A

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

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4
Q

percentage of dogs/cats with congenital PSS and MVD

A

PSS with MVD60% dogs90% cats

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5
Q

hepatic encephalopathy occurs when what percentage of the liver is dysfunctional

A

HE occurs with 70% liver function is lost

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6
Q

most important neurotoxin for HE

A

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

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7
Q

MOA of benzodiazipines and GABA for causing HE

A

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

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8
Q

MOA bile acids for causing HE

A

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

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9
Q

causes of coagulopathy in liver failure

A

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)

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10
Q

odds ratio of Yorkshire Terriers for occurrence of congenital PSS

A

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

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11
Q

other toy breeds affected with congenital PSS

A

suspect hereditary–yorkshire–maltese–cairn

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12
Q

breeds overrepresented with intrahepatic PSS

A

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

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13
Q

type of intrahepatic PSS in irish wolfhounds

A

left divisional intrahepatic PSShereditary in irish wolfhounds

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14
Q

type of intrahepatic PSS in australian shepherds

A

right divisional intrahepatic PSSoverrepresented in australian shepherds

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15
Q

MOA of PU/PD in PSS dogs

A

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

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16
Q

abdominal effusion in hepatic arteriovenous malformations in dogs

A

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)

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17
Q

preoperative GI hemorrhage reported in PSS patients

A

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

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18
Q

ptyalism reported in cats as clinical sign of PSS

A

75%

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19
Q

causes of lower urinary tract signs in PSS patients

A

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

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20
Q

clinicopathologic findings for hepatic vascular anomaly patients

A

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

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21
Q

protein C and ddx btwn PSS vs MVD

A

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

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22
Q

flow of hepatic AV malformations vs extrahepatic PSS on doppler US

A

hepatic AV malformations–hepatofugalextrahepatic PSS–hepatopedal

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23
Q

diagnostic imaging for hepatic vascular anomalies

A

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

24
Q

normal scintigraphy shunt fractions

A

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

25
Q

disadvantages of scintigraphy

A

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

26
Q

dose for intra-operative portovenography

A

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

27
Q

MOA and dose lactulose

A

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

28
Q

diuretic of choice to treat ascites from portal hypertension

A

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

29
Q

epiploic foramen

A

dorsally—caudal vena cavaventrally–portal vein caudally–celiac artery/hepatic artery

30
Q

most common area to find multiple acquired PSS

A
  1. near right kidney2. within intestines
31
Q

normal portal pressures

A

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

32
Q

ameroid constrictor material

A

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

33
Q

suture ligation of PSS

A

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

34
Q

signs of portal hypertension

A

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

35
Q

what percentage of dogs require partial shunt attenuation

A

86%

36
Q

where is the ductus venous visible

A

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

37
Q

what are portocaval windows

A

when portal vein and cava vascular walls fuse

38
Q

list post operative complications PSS

A

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

39
Q

propofol CRI for PSS post op seizures

A

0.1-1.0 mg/kg/min

40
Q

mortality rates for surgically treated EHPSS

A

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

41
Q

mortality rates for surgically treated IHPSS

A

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

42
Q

portal vein tributaries

A

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

43
Q

three types of classifications of liver vascular disease

A
  1. congenital PSS2. primary hypoplasia of portal vein (abN hepatic blood flow or portal hypertension)3. disturbances in portal outflow
44
Q

treatment for acute severe HE

A

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

45
Q

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

A

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

46
Q

prognosis for PVH-MVD (no portal hypertension)

A

excellent 90% long term survival

47
Q

prognosis for PVH with portal hypertension

A

poor 40% long term survival

48
Q

list 6 reasons for persistent post operative clinical signs

A

—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

49
Q

list 6 methods to correct PSS

A

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

50
Q

methods to find IHPSS intraoperatively

A

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

51
Q

methods for IHPSS dissection/occlusion

A

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

52
Q

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

A

TRUEMehl et al 2005 JAVMA

53
Q

complications in cats postoperative shunt occlusion

A

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

54
Q

treatment for hepatic AV malformations

A

most often seen in Right and central divisionlobectomy/resection

55
Q

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

A

true

56
Q

factors that may be negative predictors of outcome

A

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

TnJ (128 decks)

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