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Gastrointestinal (LECTURE NOTES) > Vascular Liver Diseases > Flashcards

Vascular Liver Diseases Flashcards

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1
Q

What are the 3 categories of obstruction of the venous system of the liver

A

Veno-occlusive disease
Budd-Chiari syndrome
Congestive hepatopathy

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2
Q

Where does the liver arise from embryologically

A

A diverticulum on the ventral surface gut

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3
Q

What are the 3 vessels of the liver

A

Hepatic Artery
Hepatic Vein
Hepatic Portal Vein

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4
Q

What is the function of the hepatic veins

A

To convey the blood away from the liver

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5
Q

What do the hepatic veins converge to form

A

Three large trunks draining into the inferior vena cava

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6
Q

What is the substance of the liver composed of

A

Lobules

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7
Q

What does each lobule consist of

A

A mass of hepatic cells, arranged in irregular radiating columns between which are the blood channels (sinusoids

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8
Q

What is the function of the sinusoids

A

T convey the blood from the circumference to the centre of the lobule ending in the intralobular vein

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9
Q

What does the intralobular vein drain into

A

The sublobular vein

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10
Q

What does the intralobular vein drain into

A

The sublobular vein

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11
Q

What is Budd-Chiari sundrome

A

An uncommon and potentially life-threatening condition

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12
Q

What causes Budd-Chiari syndrome

A

The obstruction of hepatic venous outflow at any level from the small hepatic veins to the junction of the IVC with the right atrium

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13
Q

BCS is more common in women. True or False

A

True

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14
Q

What is the commonest cause of of BCS

A

Intraluminal thrombosis

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15
Q

What are some of the other causes of BCS

A

Malignancy
Parasites
Abscess or cyst
vascular webs

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16
Q

how do the pathological features of BCS result

A

From the increased sinusoidal pressure that occurs with hepatic venous obstruction

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17
Q

Reduced venous perfusion and congestion result in what

A

Hypoxic damage to the liver parenchymal cells, releasing free radicals

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18
Q

What happens if the sinusoidal pressure is reduced

A

The liver function improves

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19
Q

What are the clinical features of BCS

A

Ascites
Hepatomegaly
abdominal pain

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20
Q

What has resulted in a decrease in mortality for BCS patients

A

Introduction of anticoagulation and earlier recognition of asymptomatic disease

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21
Q

What might also be present if IVC compression or thrombosis causes the disease

A

Leg oedema or venous collateral over the trunk and back

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22
Q

What is the diagnosis of BCS dependent on

A

Imaging:
Doppler US - shows hepatic vein obstruction or abnormal flow in large intrahepatic or subcapsular venous collaterals
Contrast CT allows assessment for parenchymal disease, ascites and splenomegaly

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23
Q

What is seen pathologically in BCS

A

A variable degree of parenchymal damage dependent on the location and extent of venous congestion

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24
Q

What is characteristic in the perivenular areas in BCS

A

Ischaemic necrosis and fibrosis

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25
What are the 3 main aims of managing BCS
Alleviate the obstruction Prevent extension of thrombosis Preserve hepatic function by decreasing centrilobular congestion
26
What is involved in the medical management of BCS
Control the ascites (low sodium diet, diuretics or paracentesis Prevent thrombosis extension (anticoagulation) Treat complications Investigate and treat underlying cause
27
How might restoration of hepatic blood flow be achieved by
Thrombolytic therapy (fresh thrombus) Percutaneous angioplasty Transjugular intrahepatic portosystemic shunt (TIPS) Portosystemic shunt surgery
28
What does TIPS do
Provides an alternative venous outflow tract to decompress the liver Useful as a bridge to liver transplantation and in acute situations
29
What does TIPS do
Provides an alternative venous outflow tract to decompress the liver Useful as a bridge to liver transplantation and in acute situations
30
Why is a liver biopsy not accurate in determining the prognosis of BCS
There is an uneven distribution of hepatic lesions in BCS
31
Why is a liver biopsy not accurate in determining the prognosis of BCS
There is an uneven distribution of hepatic lesions in BCS
32
What is Hepatic Veno-occlusive disease
It typically occurs after heamatopoietic stem cell transplantation but also after ingestion of pyrrolizidine alkaloids
33
What are the histological features of Veno-occlusive disease
Loss of sinusoidal endothelial cell appearance of gaps in the SEC barrier Narrowing of the sublobular and venous lumena become obliterated
34
What are some of the clinical features of Veno-occlusive disease
``` signs are symptoms develop within 3 weeks of exposure in the case of HSCT and primary those of tender hepatomegaly, fluids retention ascites jaundice RUQ pain ```
35
What are the risk factors for the development of VOD
Advanced age Presence of liver injury prior to HSCT Clotting cascade mutations
36
What is the fold standard investigation for VOD
Liver biopsy
37
What is the preventative measures against VOD
modifying the conditioning regimen in patients at increased risk of VOD Use of ursodeoxycholic acid as prophylaxis Heparin infusion may be useful but risk of bleeding is high
38
What is the treatment for VOD
Simply diuretics and sodium restriction | Repeated paracentesis may be required
39
What should be avoided in VOD
Hepatotoxic drugs
40
What is portal vein thrombosis
Occurs most commonly as a complication of cirrhosiss, particularly in decompensated disease
41
What are the 4 anatomical categories for PVT
Thrombus confined to the portal vein beyond confluence with the SMV Extension into the SMV but patent mesenteric vessels Diffuse splanchnic venous involvement with large collaterals Splanchnic involvement but extensive fine collaterals
42
What are the 4 anatomical categories for PVT
Thrombus confined to the portal vein beyond confluence with the SMV Extension into the SMV but patent mesenteric vessels Diffuse splanchnic venous involvement with large collaterals Splanchnic involvement but extensive fine collaterals
43
What does Portal cavernoma formation or cavernous transformation of the portal vein result from
The development of multiple small vessels in and around the recanalising or occluded main portal vein
44
What are some of the clinical features of a portal vein thrombosis
Acute: onset is suggested by the absence of clinical, endoscopic and radiological evidence of portal hypertension, typically thrombosis occurring
45
What is the most common complication of PVT
Variceal bleeding
46
What are the investigations required in PVT
Doppler ultrasound | Contrast CT
47
What is the management in PVT
Reserve or prevent the advancement of thrombosis and to treat the complications
48
How is variceal bleeding managed
Endoscopic therapy / medical therapy including non-selective B blockers and nitrates
49
What might be of benefit where splenomegaly causes hypersplenism
Splenectomy
50
What are the 5 main causes of congestive hepatopathy and cardiac cirrhosis
``` Ischaemic heart disease Cardiomyopathy Valvular heart disease Restrictive lung disease Pericardial disease ```
51
What is the classical pathological description of congestive hepatopathy and cardiac cirrhosis
Nutmeg liver
52
What are the clinical features of congestive hepatopathy and cardiac cirrhosis
Liver dysfunction is mild and asymptomatic | mild jaundice and RUQ pain in more severe congestion
53
What are the clinical features of congestive hepatopathy and cardiac cirrhosis
Liver dysfunction is mild and asymptomatic | mild jaundice and RUQ pain in more severe congestion
54
What are the symptoms of congestive hepatopathy and cardiac cirrhosis
Exertional dyspnoea orthopnoea angina
55
Presence of what murmur may make the liver pulsatile
Tricuspid regurgitation
56
What investigations are carried out for congestive hepatopathy and cardiac cirrhosis
Liver biochemistry: Hyperbilirubinaemia is mostly unconjugated Alkaline phosphatase is only mildly elevated Viral hepatitis serology Abdominal US with Doppler studies of the liver Liver biopsy ECG and Echo
57
What is the management for congestive hepatopathy and cardiac cirrhosis
Treating the underlying heart disease | Diuresis for jaundice and ascites
58
Liver cell injury resulting from subcritical supply of oxygen to hepatocytes is traditionally classified as what 2 things
``` Inadequate blood supply due to reduced hepatic arterial flow and or passive venous congestion (heart failure) termed ischaemic hepatitis Hypoxic insult (respiratory failure) termed hypxoc hepatitis ```
59
What is the final common pathway in ischaemic/ hypoxic hepatitis
Hepatocellular dysfunction secondary to critically low levels of oxygen for metabolic processes
60
Hypoxic injury to the liver is not reversible. True or false.
False- it is reversible
61
What are the 5 main aetiologies for hypoxic hepatitis
``` Primary heart disease Congestive heart failure Acute MI Chronic respiratory failure Circulatory shock and sepsis ```
62
What results in increased oxygen consumption or decreased oxygen availability
Hypoperfusion
63
What are some of the histological findings in hypoxic hepatitis
``` central hepatic vein congestion with centrilobular hepatic necrosis fragmentation of liver bulks polymorphonuclear cell infiltration abnormal hepatocyte complexes pyknosis disintegration of hypatocyte nuclei ```
64
What are absent which are present in other forms of hepatitis
Hyperplasia Inflammation regeneration
65
What are the clinical features of hypoxic hepatitis
Nausea and vomiting | Tender and enlarged liver
66
What are risk factors for hypoxic hepatitis
``` Acute and chronic heart failure respiratory failure sepsis prolonged hypotension toxin ingestion Heat stroke ```
67
What are the investigations involved for Hypoxic hepatitis
Diagnosis is based on clinical and biochemical criteria generally without the need for procedural intervention Transient serum enzyme elevation in conjunction with abnormal renal function and abnormalities in PT and APTT activity
68
What is the management for patients with Hypoxic hepatitis
Purely supportive and focuses on correcting the underlying conditions leading to hypotension and hypoxic and hepatic hypoperfusion

Gastrointestinal (LECTURE NOTES) (29 decks)

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