Syndromes of Cirrhosis Flashcards

1
Q

What does cirrhosis encompass?

A

Disruption of vasculature, generation of abnormal signalling, loss of function

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2
Q

Where are the four portocaval anastomoses?

A

Oesophageal and gastric venous plexus
Umbilical vein from left portal vein to epigastric venous system
Retroperitoneal collateral vessels
Hemorrhoidal plexus

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3
Q

What can happen to the portocaval anastomoses in portal hypertension?

A

Become engorged, dilated or varicosed and rupture

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4
Q

What is portal hypertension?

A

Portal vein pressure above 5-8mmHg

Portal vein-hepatic vein pressure gradient greater than 5mHg

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5
Q

What are the two main drivers for portal hypertension?

A

Increased resistance to portal flow

Increase portal venous inflow

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6
Q

What are pre hepatic causes of portal hypertension?

A

Blockage of the portal vein before the liver

Due to portal vein thrombosis or occlusion secondary to congenital portal venous abnormalities

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7
Q

What are intrahepatic causes of portal hypertension?

A

Due to distortion of the liver architecture
Presinusoidal = schistosomiasis, non-cirrhotic PH
Postsinusoidal = cirrhosis, alcoholic hepatitis, congenital hepatic fibrosis

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8
Q

What are the post hepatic causes portal hypertension?

A

Blockages of the venous outflow from the liver
Budd Chiari syndrome
Veno-occlusive disease

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9
Q

What factors contribute to hepatic carcinogenesis?

A

Recurrent hepatocyte death -> regeneration -> cellular hyperplasia -> mitogenic environment
Inflammation -> degranulation cell cycle control -> DNA damage -> mutagenic environment

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10
Q

What re the three most common causes of cirrhosis?

A

Alcohol
Hepatitis C
NASH (NAFLD)

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11
Q

What are the pathological features of compensated cirrhosis?

A

Clinically normal
Incidental finding
Lab test or imaging abnormalities
Portal hypertension may be present

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12
Q

What are the pathological features of decompensated cirrhosis?

A

Acute on chronic liver failure =
Infection, insult, SIRS
End stage liver disease =
Insufficient hepatocytes, ran out of liver

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13
Q

What are the signs of compensated cirrhosis?

A
NONE
Spider naevi 
Palmer erythema 
Finger clubbing 
Gynaecomastia 
Hepatomegaly (more likely to shrink)
Splenomegaly
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14
Q

What are the signs of decompensated cirrhosis?

A
As decompensated, plus 
Jaundice 
Ascites 
Encephalopathy 
Bruising
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15
Q

What are the four main complications of cirrhosis?

A

Ascites
Encephalopathy
Variceal Bleeding
Liver Failure

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16
Q

What are the general principles for treatment of decompensated cirrhosis?

A

Remove/treat underling cause
Look for and treat infection
Normalise physiology - particularly NaCl retention

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17
Q

What are the nutritional considerations for decompensated cirrhosis?

A

Low threshold for gluconeogenesis and muscle catabolism
Need 35-40kcal/kg
Small frequent meals and snacks encouraged
Beware of overnight fasting
Reduce dietary NaCl

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18
Q

What are the vitamin and mineral requirements for decompensated cirrhosis?

A

Vit B supplementation Thiamine mandatory - Excess alcohol intake
Calcium and Vitamin D - Osteoporosis and osteomalacia
Monitor fat soluble vitamins and supplement if needed - PSC and PBC

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19
Q

Why does ascites happen in cirrhosis?

A

Retention of sodium and water

Portal hypertension causes a hydrostatic gradient which forces fluid into peritoneal cavity

20
Q

What is the main aim in treatment of ascites?

A

Improve underlying liver disease

21
Q

What is the role of looking for and treating infection in the management of ascites?

A

Patients are at risk of spontaneous bacterial peritonitis

22
Q

What are the general principles of drug therapy in the management of ascites?

A

Diuretics - spironolactone first Avoid NSAIDs and other sodium retaining drugs
Monitor sodium levels due to other medications

23
Q

What is the role of dietary advice in the management of ascites?

A

No added sodium diet

Reduce salt intake, maintain nutrition

24
Q

If diuretics have not worked in reducing ascitic fluid, what may be considered next?

A

Paracentesis
Provides rapid relief
Risk of infection, encephalopathy and hypovolaemia

25
Q

If diuretics and paracentesis are not suitably controlling symptoms, what may be considered next?

A

TIPS (transjugular intrahepatic portosystemic shunt)
Used for resistant ascites
Most often cures ascites, or gives ascites controlled with diuretics

26
Q

What may have to be considered if ascites does not improve despite all other interventions, or SBP becomes a severe complication?

A

Liver transplantation

27
Q

What is spontaneous bacterial peritonitis?

A

Translocated bacterial infection of ascites

28
Q

What is the prognosis of spontaneous bacterial peritonitis?

A

Poor prognostic marker

29
Q

How is spontaneous bacterial peritonitis diagnosed?

A

Not obvious
Do a tap in all ascites and cell count
Neutrophil >250 cells/mm3

30
Q

What is the treatment for spontaneous bacterial peritonitis?

A

Urgent
Antibiotics and alba
Vascular isntability-terlipressin
Maintain renal perfusion

31
Q

What is hepatic encephalopathy?

A

Reversible mental confusion which accompanies cirrhosis due to a build up of toxins

32
Q

How is hepatic encephalopathy diagnosed?

A

Flap confusion
Any neurology
Alcohol withdrawal

33
Q

What is the treatment for hepatic encephalopathy?

A

Look for and treat cause
Lactulose to clear gut/reduce transit time (rifaxamin)
Maintain nutritional status with small, frequent meals and bedtime CHO
Consider transplantation if spontaneous

34
Q

What is the pathophysiology of variceal bleeding?

A

Increased hepatic resistance + portal blood flow
Increased vatical wall tension
Wall tension gets too high, varies pop

35
Q

What is the progression of variceal bleeding?

A
1/3 of varies bleed 
40-60% stop 
70-80% rebleed 
Decompensation 
Liver failure 
Death
36
Q

What are the primary prophylactic measures to prevent variceal bleeding?

A
Beta blockers (must be nonselective, so propranolol or carvideolol) 
Variceal ligation 
Regular endoscopy
37
Q

What is the pathway for acute variceal bleeding?

A

Resuscitation
Vit K, FFP and platelet transfusion to correct clotting abnormalities
Start IV terlipressin
Endoscopic therapy
If uncontrolled, Sengstaken-Blakemore tube (ballon tamponade)

38
Q

What are the two types of endoscopic therapy for variceal bleeding?

A

Sclerotherapy

Variceal Ligation

39
Q

What are the pros/cons to sclerotherapy for variceal bleeding?

A
Effective and longterm 
Intra-variceal 
Free hand and flexible 
Sclero ulcers 
Complications
40
Q

What are the pros to variceal ligation for variceal bleeding?

A

aka Banding
Quicker eradication
Lower morbidity
As effective

41
Q

What are the pros/cons to balloon tamponade for treatment of variceal bleeding?

A

80-90% success
Risks of aspiration and perforation, usually fatal
Gastric balloon only
Used for uncontrolled bleeding varies

42
Q

What are the pros/cons to TIPS for treatment for variceal bleeding?

A

Effective
Low mortality
Anyone, anytime

Encephalopathy
Blockage

43
Q

What is the secondary prophylaxis for variceal bleeding?

A

Variceal band ligation

Beta-blockers

44
Q

When might liver transplantation be considered in cirrhosis?

A

Event based = Resistant ascites, SBP, variceal bleed
Liver function based = Bilirubin, albumin, prothrombin time
QoL based = itch, lethargy, spontaneous encephalopathy

45
Q

What UKELD score must a patient have to be listed for elective liver transplant and why?

A

49 (unless they have a variant syndrome or HCC)
Equals 9% 1 year mortality, which is the same as the 1 year mortality for elective liver transplant (i.e. more likely to die if they don’t have the surgery)