hepatic vascular anomalies (Ganjei) Flashcards

1
Q

The gallbladder sits between what lobes in dog/cat?

A

Right medial and the quadrate lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the role of the hepatic artery in the liver

A

supplies 20-25% of blood volume, and 50% of O2

arises from celiac artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the role of the portal vein in the liver

A

Supplies 75-80% of blood volume to liver and 50% of O2
- portal vein drains blood from various abdominal organs (SI, stomach, spleen, colon, pancreas, rectum)

portal vein in GREEN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe flow of blood starting with portal vein and ending with the heart

A

portal vein -> liver detoxifies blood -> detoxified blood in central vv. -> main hepatic vein -> caudal vena cava -> heart

bottom: intestinal vasculature wide green branches: mesenteric arcades single green: main portal vein thin green branches: intrahepatic portal brr. two blue branches in liver: central hepatic veins singular blue branch: main hepatic vein main blue trunk: caudal vena cava
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which type of PSS usually occurs in younger animals?

A

Congenital PSS
- shunt occurs as a single intrahepatic or extrahepatic vessel (portal system directly into systemic circulation, bypassing the liver)
- majority of PSS cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which type of PSS usually occurs in older animals?

A

Acquired PSS
- shunt occurs 2º to chronic portal hypertension
- this type of PSS is a way of the body to adapt to the hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

5 types of hepatic vascular anomalies

A

1. EHPSS (congenital)
2. IHPSS (congenital)
3. Microvascular dysplasia (congenital)
4. Portal vein hypoplasia (congenital; causes multiple acquired shunts)
5. Multuple acquired shunts (acquired)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology of EHPSS

A
  • Single vessel connecting portal venous system to caudal vena cava OUTSIDE of liver parenchyma
  • Accounts for 66-75% of congenital dog/cat shunts
  • Two main types: portocaval and portozygous
  • small and toy breeds++
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathophysiology of IHPSS

A
  • Single vessel connecting portal venous system to caudal vena cava INSIDE of liver parenchyma
  • Accounts for 20% of congenital dog/cat shunts
  • Two main types: portocaval and portozygous
  • large & giant breeds++
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pathophysiology of Microvascular dysplasia (MVD)

A
  • Primary hypoplasia of portal vein without portal hypertension
  • Microscopic malformation of hepatic vasculature

only diagnosed on a micoscope slide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pathophysiology of Portal Vein Hypoplasia

A

the smaller (hypoplastic) portal vein causes increased resistance (b/c narrower vessel for blood to flow through) -> leads to portal hypertension & multiple acquired shunts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

EHPSS and MVD are more common in what size dogs?

A

Small breeds (yorkie; pugs, maltese, mini schnauzer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

IHPSS are more common in what size dogs

A

Large breeds (irish wolfhounds, retrievers, aussie shepherd and cattle dog)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

All hepatic vascular anomalies appear clinically the same. What are the most common signs?

A
  • neurologic (hepatic encephalopathy+++)
  • gastrointestinal
  • urinary
  • failure to thrive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hepatic Encephalopathy signs

A

Diffuse forebrain disease
- compulsive circling or pacing; head-pressing
- seizures
- depressed level of consiousness
- ataxia
- blindness (cats)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pathophysiology of hepatic encephalopathy

A
  • occurs when 70% of liver function is lost
  • Ammonia accumulation (GI tract is loaded with NH3 from the gut flora)
  • endogenous benzodiazepines accumulation
  • the accumulatd compounds impede neuronal and astrocyte function

(cell swelling & cerebral edema, inhibition of pumps/ion channels, elevated intracellular Ca2, depression of electrical activity, altered permeability of BBB)

17
Q

Why do some dogs with hepatic vascular anomalies develop urethral stones?

A

Accumulation of ammonia in bloodstream -> accumulation of urate in urine -> excess production of ammonium biruate stones

normally converted to urea in liver

very dilute urine

18
Q

Main findings on CBC/Chem of hepatic vascular anomaly patients

A
  • microcytosis (hypoferremia)
  • leukocytosis & neutrophilia (inadequate hepatic endotoxin clearance or chronic inflamm. state)
Serum chemistry findings
19
Q

UA findings of hepatic vascular anomaly patients

A
20
Q

Test of choice for evaluating liver function in dogs with PSS

A

Bile Acids Test

21
Q

How to differentiate between HVA and liver failure patients on bloodwork?

A
22
Q

Common findings on U/S of HVA?

A
  • decreased # of portal & hepatic vv.
  • small liver
  • anomalous vessel
  • reduced portal vein:aorta size
23
Q

Gold standard for evaluating portal system and why?

A

CT
- can differentiate b/w intra- and extra-hepatic shunts/other anomalies
- provides complete evaluation of hepatic vasculature

24
Q

How are HVAs treated?

A

ALL: medical management - recommended before ANY anesthesia is performed for dx or tx
- decrease NH3 (ammonia) absorption
- nutritional support
- hepatoprotective therapy
- hepatoprotective therapy
- GI ulceratino prevention (intrahepatic)
- tx/prevent hepatic encephalopathy

25
Q

How to decrease NH3 absorption

A
  • ABX
  • Lactulose
26
Q

HVAs: Nutritional management - diet

A

Moderately restrict protein
- 18-22% for dogs
- 30-35% for cats

source of high biologial protein

27
Q

How are GI ulcers prevented in IHPSS patients?

A

PPIs (omeprazole) - LONG term//for life!!

28
Q

When is surgery for PSS indicated?

A
  • NEVER as an emergency!
  • Only ever if medical management does not resolve signs after at least 2 weeks
29
Q

Surgical techniques for PSS

A

1. Partial or complete acute occlusion (not well-tolerated/poorer prognosis - most common post-oop complications like hemorrhage)
2. Gradual Occlusion (most common)
3. Endovascular embolization (for IHPSS)

endovascular embolization: block shunt into vena cava via catheter thru jugular vein

30
Q

Top 3 risk of PSS surgery?

A
  1. Portal hypertension (less common with gradular occlusion)
  2. Seizures (poor prognosis if they occur)
  3. Recurrence of Clinical Signs (most common chronic complication)

other: hypoglycemia

IHPSS: GI bleeding
Cats: (temporary) blindness

31
Q

Long-term prognosis of surgical intervention in dogs versus cats

A

Good-to-excellent outcome in both dogs and cats (EHPSS & IHPSS for dogs, EHPSS for cats)