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Year 5 - Gastro > Liver cirrhosis > Flashcards

Liver cirrhosis Flashcards

1
Q

What pathology occurs in liver cirrhosis?

A

Scarring of the liver

Portal hypertension

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2
Q

Causes of cirrhosis

A

Most common causes:

  • Alcoholic liver disease
  • NAFLD
  • Hep B and C

Rarer:

  • Autoimmune hepatitis
  • PBC
  • Haemochromatosis
  • Wilson’s
  • A1AD
  • CF
  • Drug causes e.g. amiodarone, methotrexate, sodium valproate
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3
Q

Signs of liver cirrhosis

A

Jaundice – caused by raised bilirubin

Hepatomegaly – however the liver can shrink as it becomes more cirrhotic

Splenomegaly – due to portal hypertension

Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away

Palmar Erythema – caused by hyperdynamic cirulation

Gynaecomastia and testicular atrophy in males due to endocrine dysfunction

Bruising – due to abnormal clotting

Ascites

Caput Medusae – distended paraumbilical veins due to portal hypertension

Asterixis – “flapping tremor” in decompensated liver disease

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4
Q

Investigations in suspected liver cirrhosis

A

Bloods - clotting, INR, LFTs, U&Es (hepato-renal syndrome), AFP (for hepatocellular carcinoma), FBC (may show thrombocytopenia)

Ultrasound

Fibroscan - to check elasticity of the liver using sound waves

Liver biopsy can be used to confirm the diagnosis of cirrhosis

Enhanced Liver Fibrosis (ELF) blood test - first line recommended investigation for assessing fibrosis in non-alcoholic fatty liver disease only, but it is not currently available in many areas

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5
Q

Scoring system for cirrhosis severity and prognosis?

A

Child-Pugh score

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6
Q

What is Child Pugh score?

A

Score based on bilirubin, albumin, INR, ascites and encephalopathy

Max score 15, minimum 5

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7
Q

What score can estimate mortality in cirrhosis?

A

MELD score - estimates 3 month mortality and helps guide referral for transplant

Formula takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis

Recommended by NICE to be used every 6 months in patients with compensated cirrhosis.

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8
Q

General management of cirrhosis

A

Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma

Endoscopy every 3 years in patients without known varices

High protein, low sodium diet

MELD score every 6 months

Consideration of a liver transplant

Managing complications e.g. hepatic encephalopathy, ascites, SBP, varices

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9
Q

What are some complications of cirrhosis?

A

Portal hypertension, resulting in:

  • Splenomegaly
  • Oesophageal varices
  • Thrombocytopenia (occurs due to sequestration of platelets in large spleen)

Ascites
SBP

Hepato-renal syndrome (pooling of blood in portal vessels causes loss of blood volume in kidneys)

Hepatic encephalopathy - build up of toxins especially ammonia

Hepatocellular carcinoma

Hypoglycaemia (significant indicator of end-stage liver disease - aren’t enough functioning hepatocytes for gluconeogenesis

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10
Q

Management of malnutrition in liver cirrhosis?

A 
Regular meals (every 2-3 hours)
Low sodium (to minimise fluid retention)
High protein and high calorie (particularly if underweight)
Avoid alcohol
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11
Q

Why do varices occur in portal hypertension?

A

Back pressure due to portal hypertension causes the vessels at sites where the portal system anastomoses with the systemic venous system to become swollen and tortuous.

These are varices

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12
Q

Management of stable varices

A

Propranolol - to reduce portal hypertension

Elastic band ligation

Injection of sclerosant (less effective than ligation)

TIPS procedure

  • IR make a connection between the hepatic and portal vein
  • Relieves pressure
  • Used if medical/endoscopic treatments fail or if there are bleeding varices that cannot be controlled in other ways.
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13
Q

Management of bleeding varices

A

Resuscitation:

  • Terlipressin can slow bleeding
  • Correct coagulopathy
  • Prophylactic broad spectrum antibiotics

Urgent endoscopy with:

  • Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
  • OR Elastic band ligation of varices
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14
Q

If endoscopy treatments of bleeding varices fail?

A

Sengstaken-Blakemore Tube is an inflatable tube inserted into the oesophagus to tamponade the bleeding varices.

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15
Q

What causes ascites in cirrhosis?

A

Increased pressure in the portal system causes fluid to leak out of capillaries into peritoneal cavity

Cirrhosis causes a transudative ascites (low protein content)

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16
Q

Management of ascites

A

Low sodium diet

Anti-aldosterone diuretics (spironolactone)

Paracentesis (ascitic tap or ascitic drain)

Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid

17
Q

What can be considered in refractory ascites?

A

TIPS procedure

Liver transplant

18
Q

When are prophylactic antibiotics given in ascites to prevent SBP?

A

If less than 15g/litre of protein in the ascitic fluid

19
Q

What is SBP?

A

Infection of ascitic fluid without clear cause

I.e. not secondary to an ascitic drain or bowel perforation

20
Q

How does SBP present?

A

Can be asymptomatic so have a low threshold for ascitic fluid culture

Fever

Abdominal pain

Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)

Ileus

Hypotension

21
Q

Most common causative organisms of SBP?

A

Escherichia coli

Klebsiella pnuemoniae

Gram positive cocci (such as staphylococcus and enterococcus)

22
Q

Management of SBP

A

Ascitic culture before antibiotics

Usually treated with an IV cephalosporin e.g. cefotaxime

23
Q

What is hepatorenal syndrome?

A

Pooling of blood in portal system leads to hypotension in the kidneys

RAAS is activated causing renal vasoconstriction

Rapidly deteriorating renal function

Hepatorenal syndrome is fatal within a week or so unless liver transplant is performed.

24
Q

What is hepatic encephalopathy?

A

It is thought to be caused by the build up of toxins that affect the brain especially ammonia

Ammonia builds up as liver impaired so not effectively metabolised

Ammonia is produced by intestinal bacteria and absorbed in the gut

25
Q

Precipitating factors for hepatic encephalopathy

A 
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (particularly sedative medications)
26
Q

Management of hepatic encephalopathy

A

Laxatives e.g. lactulose - first line

  • Promote excretion of ammonia (before it is absorbed by intestine)
  • Aim 2-3 stools/day

Antibiotics - rifaximin - reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.

Nutritional support - may need NG feeding

Year 5 - Gastro (15 decks)

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