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acute & critical care cc > 6. Liver Cirrhosis > Flashcards

6. Liver Cirrhosis Flashcards

1
Q

What is cirrhosis?

A

Chronic inflammation damaging liver tissue, causing it to be replaced by scar tissue (fibrosis) and nodules of scar tissue form

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2
Q

What is portal hypertension?

A

Resistance to blood flow into the liver due to scar tissue formation

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3
Q

What are the four most common causes of liver cirrhosis?

A

Alcoholic liver disease

Non-alcoholic fatty liver disease

Hepatitis C

Hepatitis B

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4
Q

Apart from ALD, NAFLD, Hep B/C, list 7 causes of cirrhosis.

A

Auto-immune hepatitis

Cystic fibrosis

Primary biliary cirrhosis

Haemochromotosis

Wilson’s disease

Alpha 1 anti-trypsin deficiency

Drugs: methotrexate, sodium valproate, amioderone

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5
Q

2 SS specific to decompensated liver cirrhosis

A

Asterixis (flapping tremor) as sign of toxin build up and will cause encephalopathy

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6
Q

In severe cirrhosis, what do UE show?

A

Hyponatremia indicating sodium retention

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7
Q

What disease is monitored for in pts with cirrhosis and in what 2 ways, including how regularly?

A

HCC

Alpha-fetoprotein blood test (every 6m)

US (every 6m)

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8
Q

What is the ELF blood test?

A

Enhanced Liver Fibrosis blood test

First line investigation for assessing fibrosis in NAFLD

Measures 3 markers (HA, PIINP and TIMP-1) and uses an algorithm to generate a score

Mild/ none fibrosis: Less than 7.7

Moderate fibrosis: 7.7 to 9.8

Severe: 9.8+

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9
Q

How does cirrhosis present on US?

A

Nodularity

Corkscrew appearance of arteries

Enlarged portal vein with reduced flow

Ascites

Splenomegaly

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10
Q

According to NICE, who should be given a fibroscan to assess for cirrhosis every 2y?

A

Anyone at risk:

  • Hep C (if have hep B assess yearly)
  • Heavy OH drinkers (men 50+ units, women 35+ units)
  • ALD
  • NAFLD + evidence of fibrosis on ELF blood test
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11
Q

Which scoring systems are used to evaluate cirrhosis?

A

Childs-Pugh score: bilirubin, INR, albumin, ascites and encephalopathy are given a score or 1, 2, 3 each and score out of 15 indicates severity and prognosis

MELD score: used every 6m in patients with compensated cirrhosis, gives estimated 3m mortality and whether they need a transplant or dialysis

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12
Q

General management of cirrhosis

A

US and AFP every 6m for HCC

Endoscopy every 3y in pts w/ varices

High protein, low sodium diet

MELD score every 6m

Consider transplant

Manage complications

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13
Q

List the complications of cirrhosis

A

Malnutrition

Portal hypertension and varices

Ascites and spontaneous bacterial peritonitis

Hepato-renal syndrome

Hepatic encephalopathy

Hepatocellular carcinoma

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14
Q

Why does cirrhosis cause malnutrition and how is it managed?

A

Cirrhosis means the liver can’t metabolise proteins and less protein is produced

Cirrhosis prevents glycogen storage and release as glucose

So muscle is used for fuel instead leading to wasting and weight loss

Managed:
Regular meals (every 2-3h)
Low sodium diet to limit fluid retention
High protein and high calorie diet
Avoid OH
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15
Q

The portal vein comes from which 2 veins?

A

Superior mesenteric and splenic

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16
Q

Where does PVH cause variceal formation and give 4 examples.

A

Where the portal system anastomoses with systemic system, varices form:

Gastro-esophageal junction

Iliocecal junction

Rectum

Anterior abdominal wall via umbilical vein (caput medusa)

17
Q

How are bleeding esophageal varices treated, including the 2 aspects?

A
  1. Resuscitation

Slow bleeding with vasopressin analogues such as terlipressin

Slow bleeding with propanolol

Correct any liver disease induced coagulopathy with Vit K and FFP (contains clotting factors)

Prophylactic broad-spectrum a/b reduce mortality

Esophageal varices can exsanguanite rapidly and become life threatening so consider intubation and ICU

  1. Urgent endoscopy

Inject with sclerosant to cause inflammatory obliteration

Elastic band ligation of varices

If above fail, Sengstaken-Blakemore tube inserted into esophagus to tamponade bleeding varices (balloon inflated to restrict blood flow to esophagus)

Last-line: TIPS

18
Q

What kind of ascites does cirrhosis cause?

A

Transudative (low protein)

19
Q

How does cirrhosis cause ascites?

A

High pressure in portal system

Fluid forced out of capillaries in liver and bowel

Fluid builds up in peritoneal space

20
Q

How can ascites cause AKI?

A

Lose circulating volume to peritoneal space

Renal hypoperfusion aka pre-renal cause of AKI

21
Q

How does ascites activate the RAAS and what does this system do?

A

Kidneys detect low circulating volume

Release renin

Renin converts angiotensinogen to angiotensin 1

A1 gets converted into A2 by ACE in lungs

A2 causes aldosterone to be released, vasoconstriction and ADH to be released

Aldosterone causes sodium and water retention so circulating volume increases (also causes renal artery vasoconstriction to increase bp in kidneys)

22
Q

Describe the management of ascites

A

Low sodium diet to prevent water retention

Spironolactone (potassium sparing diuretic)

Paracentesis via ascitic tap or drain

If have under 15g/L of protein in peritoneal fluid, give prophylactic a/b (ciprofloxacin or norfloxacin) for SBP

For refractory ascites consider TIPS or transplantation

23
Q

What is spontaneous bacterial peritonitis?

A

When an infection develops in the peritoneal lining and fluid w/o any clear cause (not secondary to bowel perforation or infection due to ascitic drain)

24
Q

SS of SBP

A

Can be asymptomatic - so have low threshold for getting ascitic fluid culture

Hypotension

Fever

Ab pain

Ileus (temporary lack of normal intestinal muscle contraction)

25
Q

What blood results would indicate SBP?

A

Raised WCC

Raised CRP

Raised creatinine

Metabolic acidosis

26
Q

Which 3 organisms most commonly cause SBP?

A

E.coli

Klebsiella pneumoniae

Gram positive cocci: staphylococcus or enterococcus

27
Q

Prophylactic a/b given for patients with low protein ascites are ciprofloxacin or norfloxacin. How is SBP managed?

A

Take ascitic fluid sample for culture

IV cephalosporin such as cefotaxime

28
Q

Describe hepato-renal syndrome

A

Fatal within a week w/o transplant

PVH leads to blood pooling in portal veins, reducing circulation elsewhere

Kidneys activate RAAS and cause renal artery vasoconstriction

Vasoconstriction + low circulating volume = kidney starved = AKI and rapidly deterorating kidney function

29
Q

Describe hepatic encephalopathy aka portosystemic encephalopathy and explain the role of ammonia in it

A

Liver stops functioning

Toxins build up

Ammonia builds up in particular

Made in gut by intestinal breakdown on protein break-down and absorbed by gut

In cirrhosis liver can’t metabolise ammonia and collateral vessels form between portal and systemic circulation, so ammonia can bypass the liver

30
Q

Management of hepatic encephalopathy

A

Laxatives (lactulose) to clear ammonia from gut before it enters systemic circulation. Aim for 2-3 soft motions/d. Enemas may be required initially.

A/B (rifaximin) to reduce the amount of bacteria in the gut so less ammonia produced

Nutritional support (may need nasogastric feeding)

31
Q

SS of HE

A

Acute: reduced consciousness and confusion

Chronic: personality, memory and mood changes

32
Q

Percipitating HE factors

A

Constipation

Electrolyte disturbance

Infection

GI bleed

High protein diet

Medications (particularly sedative)

33
Q

In cirrhosis, which tests should be done?

A

Viral markers

Auto-antibodies

acute & critical care cc (6 decks)

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