liver circulatory disorder - Állatorvostudományi egyetem · liver circulatory disorder ascites...
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2017.11.15.
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Liver circulatory disorder
Ascites
Dr. Sterczer Ágnes Department of Internal Medicine, University of Veterinary Medicine
Liver blood supply
Afferent dual
Hepatic portal vein 70-80% of blood, and 50% of oxygen
Collect blood from the intestine
Separates into two main branches, entering at hilus Right:supplies the right side of liver
Left: supplies the left + central portion
Hepatic artery 20-30% of afferent blood, but 50% of oxygen
Branches accompany the portal vein
Efferent single
Hepatic veinvena cavaheart
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Liver structure with blood supply
•Terminal branches end into the
periportal sinusoids
•Connect with sinusoidal system
•Sinusoidal blood enters
central vein=terminal hepatic vein
in the liver lobule
•Central veins drain into branches
of hepatic vein
•Caudal vena cava heart
TYPES OF LIVER CIRCULATORY DISORDERS
Alterations in prehepatic supply (v. portae, a. hepatica)
changes in portal (v. portae) blood supply
: following food ingestion, enteritis
active hyperaemia of the liver
: decrease of portal blood flow: CPSS;
portal vein hypoplasia, thrombosis
changes in arterial (a. hepatica) blood supply
: when portal blood flow is insufficient; compensatory!
: hepatic venous congestion
impaired function of the left-side heart, (or rarely
thrombosis, tumors of the hepatic arteries)
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TYPES OF LIVER CIRCULATORY DISORDERS
Alterations in intrahepatic circulation
"Portal hypertonia" often develops alone or with ascites but NOT with general edema
Causes:
congenital anomalies
persistent arterio-venosus fistula
intrahepatic portosystemic shunts (CIPSS)
intrahepatic vascular resistance (diffuse hepatic)
chronic hepatitis, cirrhosis, neoplasms, swelling of hepatocytes
Compensation: acquired portosystemic shunting CNS signs
TYPES OF LIVER CIRCULATORY DISORDERS
Alterations in posthepatic circulation
v. hepatica, v. cava caudalis, right-side heart
Increased outflow: theoretical situation
Decreased outflow
Cause: passive hyperaemia (congestion) of the
liver induration, fibrosis („nutmeg liver”)
Obstruction of v.hepatica or v.cava /right side
heart failure /pericardial disease
Portal hypertonia is common with edema & hydrops in
body cavities)
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Pathophysiology
Development of portal hypertension Common in chronic hepatitis in dogs
(rare in cats)
↑resistance to blood flow
←fibrosis, contraction of Stellate
(hepatocyte swelling, infiltration) Consequences
Ascites APSS GI wall congestion and oedema
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Ascites
Ascites is a pathological accumulation of free fluid within a the peritoneal cavity Strictly, ascitic fluid is serous in nature and is classified, depending on its protein and cellular content composition into following categories:
Transudate, modified transudate, exudate
Ascites
Courtesy of Dr.K.Voros
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Ascites
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ASCITES Abdominal effusion /fluid of low protein and low cell count
Transudate:
Pure: cell:< 2500/ l protein:<2,5 g/dl <1016 clear
Chronic hepatic failure+alb / intrahepatic portal vein hypoplasia / portal vein thrombosis
Modified: cell:< 7000/ l protein:2,5 g/dl 1016-1031 Chronic hepatic failure / heart failure / pericardial disease / caval
syndrome
Exudate: septic / nonseptic
high cellularity, high protein
Endothelial cell-lined sinusoids are highly permeable:
Hepatic lymph: high protein, hypo-moderate cellular
Intestinal lymph: low protein, hypocellular
Ascites in patients with hepatic disease: portal hypertension (CH, cirrhosis, portal vein hypoplasia, LDH) + alb +renal retention of salt and H2O
ASCITES Prehepatic
Intestinal lymph: low protein /hypocellular (pr; cell)
portal flow + high intrahepatic vascular resistance
AV fistula / v. portae hypoplasia / v. portae obstruction
Intrahepatic Presinusoidal
Intestinal lymph (pr; cell)
Periportal fibrosis / portal venule hypoplasia Sinusoidal
Hepatic +(intestinal) lymph (pr/; cell)
Cellular (inflamm, neoplastic), collagen infiltrates Postsinusoidal
Hepatic +(intestinal) lymph (pr/; cell)
Hepatic venular fibrosis
Posthepatic
Hepatic lymph (pr ; cell)
Passive congestion Obstruction of v.hepatica or v.cava /right side heart failure
/pericardial disease
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ascites, caused by hypoproteinemia due to insufficient protein supply True transudate
Modified transudate, due to
right heart failure
858c.tif
860a.tif
Courtesy of Dr.K.Voros
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CAUSES AND PATHOGENESIS OF ASCITES
Causes:
1.
2.
3.
4.
Portal hypertonia
Hepatic lymph production increasesmechanical factors
Hypoalbuminaemia
Hypovolaemia, hyperosmosisfunctional factors
increased aldosterone and ADH release
Pathogenesis:decreased albuminsynthesis
intrahepatic obstruction ofcapillaries
decreasedoncotic pressure
impaired venousoutflow
portal hyper-tension
increased lymphproduction
ASCITES
hypovolaemia
aldosterone production increased inactivation ofaldosterone decreases
Na+ and water retention in thetubuli increases
inactivation of ADHdecreases
CAUSES AND PATHOGENESIS OF ASCITES
Causes:
1.
2.
3.
4.
Portal hypertonia
Hepatic lymph production increasesmechanical factors
Hypoalbuminaemia
Hypovolaemia, hyperosmosisfunctional factors
increased aldosterone and ADH release
Pathogenesis:decreased albuminsynthesis
intrahepatic obstruction ofcapillaries
decreasedoncotic pressure
impaired venousoutflow
portal hyper-tension
increased lymphproduction
ASCITES
hypovolaemia
aldosterone production increased inactivation ofaldosterone decreases
Na+ and water retention in thetubuli increases
inactivation of ADHdecreases
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Liver cirrhosis
Courtesy of Cs. Jakab
Courtesy of Cs. Jakab
Courtesy of Cs. Jakab
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Vascular liver diseases PSS
CPSS
APSS
Portal vein hypoplasia
Primary hypoplasia of portal vein PHPV
Hepatic microvascular dysplasia HMD (mild)
Idiopathic noncirrhotic PH
Hepatoportal fibrosis
Secondary hypoplasia of portal vein
Occlusion of portal vein
Hepatic arterio-venous fistula Hepatic venous outflow obstruction
Budd-Chiari LIKE syndrome
PH
Portosystemic shunts (PSS)
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Healthy state
Heart
Caudal vena cava
Portal vein
Forms of extra- and intrahepatic PSS
Intrahepatic shunt Extrahepatic shunts
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PORTOSYSTEMIC SHUNT PSS is an abnormal vascular communication
between the portal and systemic venous
systems allow portal blood to reach the systemic circulation
without first passing through the liver increased level of enterically derived toxins in the
systemic circulation
(NH3, mercaptan, SCFA, AAA, GABA)
hepatic atrophy decreased hepatic blood flow
lack of hepatotropic factors
Congenital or acquired
PORTOSYSTEMIC SHUNT
CONGENITAL
Intrahepatic
Extrahepatic
AQUIRED
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Congenital PSS anomalous embryonal vessels
short, wide
soliter / single
75% of PSS
usually in < 1 year old animal
portal hypotension
intra or extrahepatic
Intrahepatic PSS always soliter persistent ductus venosus • d. venosus fetal connection v. umbilicalis v. c. c.
• d. venosus is closed functionally in 3 days, anatomically 15-18 days after the born
left, central, right divisional Left division: morphology is consistent with failure
of fetal ductus venosus to close
large-breed dogs Irish wolfhounds, Golden Retriever, Irish Setters, Labrador Retriever, old english sheepdog, German Shepherd
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Extrahepatic PSS always soliter
anatomically abnormal communication between the portal (v. portae, v. gastrolienalis, v. gastroduodenalis, v. mesenterica) and the v. cava caudalis or v. azygos
small-breed and toy dogs, cats (Eu: Yorkshire terrier, Cairn terrier, Shih Tzu, Maltese Terrier, Pug, Mini Schnauzer USA: Yorkshire terrier, Poodle, Mini Schnauzer)
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Aquired PSS multiplex, collateral vessels narrow, twisting, tortuous protective compensatory response to PH
reopening of the existing, but not functioning extrahepatic portocaval or portoazygos anastomosis
portal hypertension (chronic, severe diffuse: cirrhosis, CH, neoplasm, LDH; AVF, PVH)
usually in older animals
not every portal hypertension cause PSS, a different between the blood pressure is necessary Posthepatic PH no APSS (portal and systemic
pressure)
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Hepatic encephalopathy
Hepatocerebral syndrome
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metabolic dysfunction of the brain secondary to liver dysfunction
Acute HE 10% rare -acute, fulminant encephalopathy, caused by sudden, almost complete necrosis of liver
Chronic HE 90% common
PSS collateral circulation + impaired liver function
Portosystemic encephalopathy (PSE) PSE chronic HE PSVA congenital
aquired
HEPATIC ENCEPHALOPATHY HE
HEPATIC ENCEPHALOPATHY dog: PSS + liver function • huge reserve capacityprevents the development of HE even in
severe parenchymal liver disease not accompanied by PSS
very rarely congenital urea cycle enzyme deficiency
cat: PSS+ liver function
Hepatic lipidosis: arginin (anorexia) less reserve,+ can not synthesize arginin in the liver
(intermediate in the urea cycle), inadequate NH3 detoxification
Portosystemic vascular anomalia is required
PORTOSYSTEMIC ENCEPHALOPATHY PSE
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Pathogenesis of PSE
Glutamate neurotransmission and NH3
GABA/benzodiazepin receptor complex
Deranged catecholaminerg neurotransmitter system
Liver
AAA
Neuron
Tyr
Dopa
Dopamin
Noradrenalin
Tyr
Tyramin
Oktopamin
Phe
B-phe
AAA
Trp
Phe
Tyr
HE: BCAAAAA
„FALS NEUROTRANSMITTER”„FALS NEUROTRANSMITTER”
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Hepatic encephalopathy
CNS signs
CPSS 80-90%
episodic (few bad days alternating normal period) and the intensity, severity of the signs is wavy
precipitated by a protein rich meal
lack of correlation between blood NH3 level and severity of encephalopathic signs
HE grade (1-4)
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Vascular liver diseases PSS
CPSS
APSS
Portal vein hypoplasia
Primary hypoplasia of portal vein PHPV
Hepatic microvascular dysplasia HMD (mild)
Idiopathic noncirrhotic PH
Hepatoportal fibrosis
Secondary hypoplasia of portal vein
Occlusion of portal vein
Hepatic arterio-venous fistula Hepatic venous outflow obstruction
Budd-Chiari LIKE syndrome
PH
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Arterioportal fistulae (APF) a. hepatica—portal vein Congenital (hemangioma)
Vascular connection, allow blood to bypass the hepatic inusoidal network, flow retrograde into portal system
Clin: -young dogs (<1,5 y)
APF PH, ascites, APSS, splanchnic vascular congestion Macroscopic: large, thin-walled, tortuous, pulsating vascular channel
distorts the involved liver lobes, elevates the hepatic capsule
Continuous murmur (fremitus) turbulent blood flow over affected liver lobe
US: hepatic AV fistula
extremely dilated, tortuous, anechoic portal branch in a liver lobe=pathognomic finding
High arterial pressure dilatation of affected portal branch and hepatofugal flow
Thanks for your attention!