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Clinical > The Syndrome of Cirrhosis > Flashcards

The Syndrome of Cirrhosis Flashcards

1
Q

Liver cells that lay down fibrosis?

A

Hepatic stellate cells

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2
Q

2 main problems in liver cirrhosis?

A

Loss of functions due to there not being enough hepatocytes

Disruption of normal blood flow to and from the liver

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3
Q

Which veins drain into the portal system?

A

Superior mesenteric
Splenic vein
Gastric vein
Part from the inferior mesenteric

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4
Q

How does blood flow through the liver?

A

Oxygenated blood from hepatic artery + nutrient-rich, deoxygenated blood from the hepatic vein
Meet at the liver sinusoids

Goes into the:
Central vein
Hepatic vein
IVC

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5
Q

How does blood flow from the hepatic portal vein to the IVC?

A

There is a very low pressure in the hepatic vein (5-3 mmHg) with only a small gradient across the liver to the hepatic vein, which returns the blood to the IVC

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6
Q

What are the 4 anastomoses between the portal venous system and the systemic venous system?

A

Oesophageal and gastric venous plexus

Umbilical vein from the left portal vein to the epigastric venous system

Retroperitoneal collateral vessels

Hemorrhoidal venous plexus

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7
Q

Effects of portal hypertension on the anastamoses between the portal venous system and systemic venous system?

A

May become engorged, dilated or varicosed

Leads to rupture

ADD PICTURE 2

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8
Q

What is portal hypertension?

A

Pressure above the normal range of 5-8 mmHg

OR

A gradient of greater than 5 mmHg between the portal and hepatic veins

This represents an increase in hydrostatic P within the portal vein

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9
Q

2 causes of portal hypertension?

A
  1. Increased resistance to portal flow (R)
  2. Increased portal venous inflow (Q)

The change in pressure is equal to Q x R

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10
Q

How does cirrhosis affect the vasculature?

A

Leads to impaired hepatocellular and sinusoidal hypertension and portal-systemic shunting

Response is release of vasodilators; this decreases resistance (splanchnic and peripheral vasculature) also decreases blood volume

There is an increase in RAAS, sympathetc and ADH activity

Sodium and water retention leads to ASCITES

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11
Q

Classification of portal hypertension causes?

A
  1. Prehepatic - block of the portal vein before liver
  2. Intrahepatic - due to distortion of the liver architecture; this is either:
    Pre-sinusoidal
    OR
    Post-sinusoidal, e.g: cirrhosis, alcoholic hepatitis
    Also, budd-chiari syndrome
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12
Q

Pathway of hepatic carcinogenesis?

A

Recurrent hepatocyte death leads to regeneration that is recurrent and a mitogenic environment

Inflammation leads to deregulation of cell cycle control and DNA damage, from reaction oxygen and nitrogen species, etc
There may be other reasons, e.g: integration of Hep B viral DNA into self cells

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13
Q

When does hepatic carcinogenesis mostly occur?

A

When there is liver cirrhosis, for one reason or another

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14
Q

2 types of liver cirrhosis?

A

Compensated cirrhosis

Decompensated cirrhosis

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15
Q

Describe the presentation and diagnosis of compensated cirrhosis

A

Clinically, they are normal and it is usually and incidental finding
Portal hypertension may also be present

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16
Q

Describe the two presentations of decompensated cirrhosis

A

Liver failure:
Acute on chronic (can be pushed over the threshold by an acute event, e.g: infection, insult)
End stage liver disease - eventually, there will be insufficient hepatocytes

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17
Q

Signs of compensated cirrhosis?

A 
Spider naevi (press in centre; positive test if all of the spider legs blanch)
Palmar erythema
Finger clubbing
Gynaecomastia
Hepatomegaly
Splenomegaly

May be no signs

18
Q

Signs of decompensated cirrhosis?

A 
Jaundice
Ascites
Encephalopathy 
Bruising 
Leukonycia (extended white of nails)
19
Q

Complication of cirrhosis?

A

Ascites (appearance of this is a marker of poor prognosis)
Encephalopathy
Variceal bleeding
Liver failure

20
Q

General principles of treating decompensated cirrhosis?

A

Remove/treat the underlying cause
Look for and treat infection
Avoid NaCl retention (they are already retaining Na+)
Low threshold to switch to gluconeogenesis and lipolysis and catabolism

21
Q

Nutritional recommendations in decompensated cirrhosis?

A

Small frequent meals and snacks to reduce fasting gluconeogenesis and muscle catabolism; beware fasting over night

22
Q

Common complications of decompensated liver cirrhosis, and there causal diseases, and how to prevent this?

A

Osteoporosis and osteomalacia are common - supplement with calcium and vitamin D

Vitamin B supplementation (thiamine) is required in excess alcohol intake

In Primary Sclerosing Cholangitis and in Primary Biliary Cirrhosis, they may develop a vitamin deficiency in fat-soluble vitamins, so monitor and supplement

23
Q

Diagnosing ascites?

A

Shifting dullness when lying on back and side

Ascites on ultrasound

24
Q

Treatment of ascites?

A

Improve underlying liver disease and look for and treat infection, e.g: spontaneous bacterial peritonitis

Drugs; ensure they are not taking NSAIDs and think of the Na+ load if they are on IV

Give diuretics, but spironolactone first

Reduce salt intake but maintain nutrition; no added sodium diet

Paracentesis

TIPSS (Transjugular Intrahepatic Porto-Systemic Shunt) - an aritificial vein connects the portal vein to the hepatic vein

Transplantation

25
Q

Does abstaining from alcohol improve alcohol-related cirrhosis with ascites?

A

Yes; abstinence means 3/4 survive at 3 years

26
Q

Describe sodium balance

A

Input (from diet) - output (urine + insensible)

27
Q

Why is spironolactone used before diuretics in liver cirrhosis, but not in heart failure)

A

There is more aldosterone released in liver cirrhosis

28
Q

Treating patients with spironolactone for ascites?

A

In new ascites - escalate spironolactone
In recurrent ascites - increments of spironolactone and loop diuretic

Monitor U&E frequently

29
Q

Problems with ascities paracentesis?

A

Risk of infection
Encephalopathy
Hypovolaemia

30
Q

What is hepatic encephalopathy?

A

Confusion/altered level of consciousness due to toxin build-up, e.g: ammonia generated in the intestine, from nitrogenous compounds, is shunted past the liver into the systemic circualtion

Diagnosed by looking for flap confusion, any neurological symptoms and alcohol withdrawal

31
Q

Treatment of hepatic encephalopathy?

A

Look for cause, e.g: infection, metabolic, drugs, liver failure, and treat the cause

Lactulose (Rifaxamin) clears the gut and reduces transit time

Maintain nutritional status with small, frequents meals

If it was spontaneous, consider transplantation

32
Q

What is Spontaneous Bacterial Peritonitis (SBP) and how is it diagnosed?

A

Translocated bacterial infection of ascites
Percuss all ascites
Neutrophil count > 250 cells/mm3

33
Q

Treatment of SBP?

A

Urgent:
Antibiotics
Vascular-instability terlipressin (vasoconstrictive and improve renal perfusion)
Maintain renal perfusion

34
Q

What is varices oesophageal?

A

Bleeding as a consequence of portal hypertension and can also occur in other anastamoses

35
Q

Pathophysiology of variceal bleeding?

A

Portal hypertension causes an increase in varix size and decreased wall thickness, leading to increased variceal wall tension

36
Q

Prophylaxis of variceal bleeds?

A

Using endoscopy, check for varices; if the patient has them:

Non-selective β-blockers, like propranolol and carvidelol

Variceal ligation sometimes

If they are bleeding, give terlipressin

37
Q

Endoscopic therapies available for varices?

A

Sclerotherapy (injection that hardens tissue)

Variceal ligation - this is banding that has quicker eradication; if this does not work, balloon tamponade can be used

38
Q

Complications of balloon tamponade?

A

Aspiration
Perforation
TIPSS (stops bleeding by shunting blood from the portal to the hepatic vein)

39
Q

Secondary prevention of variceal bleeding?

A

β-blockers

Variceal band ligation

40
Q

When to consider liver transplantation?

A

If patient has significant risk and if UKLED score is over 49 (takes into account INR, creatinine, bilirubin and Na+)

41
Q

Which patients is UKELD not useful for?

A

Those with variant syndrome, e.g: chronic hepatic encephalopathy, polycystic liver disease, primary hyperlipidaemia, etc - have a bad prognosis but the score is not high enough

Hepatic cellular carcinoma

Clinical (54 decks)

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