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8. Liver & Co > Liver Cirrhosis + Portal hypertension + SBP + Hepatic encephalopathy > Flashcards

Liver Cirrhosis + Portal hypertension + SBP + Hepatic encephalopathy Flashcards

1
Q

What is cirrhosis?

A

Not a specific disease; it is an end-stage of all progressive chronic liver diseases resulting from liver cell necrosis + fibrosis, leading to impaired hepatocyte function + loss of liver architecture.

Once fully developed = irreversible!!

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2
Q

Give 3 causes of cirrhosis.

A
  1. Chronic alcohol abuse
  2. Hepatitis B and C.
  3. NAFLD
  4. Any chronic liver disease e.g. autoimmune, metabolic, vascular etc.
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3
Q

List 3 chronic liver diseases that can cause cirrhosis.

A
  • Hereditary Haemachromatosis
  • Alpha1-antitrypsin deficiency
  • Budd-Chiari
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
  • Autoimmune hepatitis
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4
Q

List 2 drugs that can cause cirrhosis.

A

Drugs - amiodarone, methyldopa, methotrexate.

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5
Q

Give 7 signs of cirrhosis.

A
  1. Jaundice – caused by raised bilirubin
  2. Bruising - due to abnormal clotting
  3. Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
  4. Leuconychia - white discolourations on nails due to hypoalbuminaemia
  5. Clubbing
  6. Dupuytren’s contracture
  7. Xanthelasma - yellow fat deposits under skin usually around eyelids
  8. Palmar Erythema – caused by hyperdynamic cirulation
  9. Ascites + abdominal pain
  10. Gynaecomastia and testicular atrophy in males - due to endocrine dysfunction
  11. Asterixis – “flapping tremor” in decompensated liver disease
  12. Caput Medusae – distended paraumbilical veins due to portal hypertension
  13. Hepatomegaly – however, the liver can shrink as it becomes more cirrhotic
  14. Splenomegaly – due to portal hypertension
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6
Q

What collagen type is deposited in the liver in cirrhosis?

A

type 1 and 3

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7
Q

What are the 2 types of cirrhosis?

A
  1. Micronodular cirrhosis
  2. Macronodular cirrhosis
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8
Q

What is the difference between micronodular and macronodular cirrhosis?

A

Micronodular - uniform involvement of liver and regenerating nodules; Often caused by alcohol or biliary tract disease

Macronodular - variable nodule size, normal acini within, tends to follow hepatitis; Often caused by chronic viral hepatitis

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9
Q

What is the Child-Pugh classification?

A

Ascites, encephalopathy, (high) bilirubin, (low) albumin and (long) prothrombin given 1-3 and added up to give a score.

Therefore: the minimum score is 5 and the maximum score is 15. The score then indicates the severity of the cirrhosis and the prognosis.

  • < 7 is best and > 10 is sign of bad prognosis
  • Risk of variceal bleeding is high if > 8
  • Can also be used to predict mortality and need for liver transplant
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10
Q

What is the gold standard for cirrhosis diagnosis?

A

Liver biopsy
- Confirms diagnosis and type and severity of disease.

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11
Q

What would you seen on a liver biopsy of a patient with cirrhosis?

A

Irregular nodules of fibrous tissues.

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12
Q

What feature seen on liver biopsy is diagnostic of cirrhosis?

A

Nodular regeneration.

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13
Q

What would LFTs show for cirrhosis?

A

LFTs:
* Serum albumin and prothrombin time are best indicators of “synthetic function” of the liver.

  • Low albumin level and long prothrombin time
    (the longer it is, the more severe/worse the synthetis liver function)
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14
Q

What can be seen in the bloods for sodium + serum creatinine for cirrhosis?

A
  1. Serum electrolytes: low Na+ (hyponatraemia)
    - Indicates fluid retention in severe liver disease
  2. Raised serum creatinine and urea
    - Become deranged in hepatorenal syndrome.
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15
Q

What can be seen in ultrasound imaging for cirrhosis?

A
  • Ultrasound:
  • Shows change in size and shape of liver - hepatomegaly (small
    liver in severe disease)
  • Marginal nodularity of the liver surface
  • Distortion of the arterial vascular architecture = “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
  • Enlarged portal vein with reduced flow
  • Ascites
  • Splenomegaly
  • Good for detecting hepatocellular carcinoma
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16
Q

What can be seen in CT imaging for cirrhosis?

A

CT:
- Hepatosplenomegaly
- Hepatocellular carcinoma

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17
Q

What can be seen in MRI imaging for cirrhosis?

A

MRI:
- Detects tumours

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18
Q

What would an endoscopy detect for cirrhosis?

A

Endoscopy:
- Detection of varices and portal hypertensive gastropathy

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19
Q

If there was alpha-fetoprotein present in the serum of a cirrhosis patient, what would you suspect to be the cause of their cirrhosis?

A

Hepatocellular carcinoma

Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma.

Can be checked every 6 months as a screening test in patients with cirrhosis along with ultrasound.

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20
Q

What is seen histologically for cirrhosis?

A

Loss of normal hepatic architecture with bridging
fibrosis and nodular regeneration

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21
Q

What is the MELD score?

A

The MELD score is recommended by NICE to be used every 6 months in patients with compensated cirrhosis.

It is a formula that takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis.

It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant.

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22
Q

What medications should be avoided when treating cirrhosis?

A

NSAIDs, opiates, sedatives

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23
Q

What is the treatment of liver cirrhosis?

A
  1. Deal with the underlying cause e.g. stop drinking alcohol.
  2. Nutrition - high protein, low sodium diet.
  3. Screening for HCC.
  4. Colestyramine for pruritus.
  5. Consider liver transplant.
  6. Managing complications.
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24
Q

List 4 possible complications of cirrhosis.

A
  1. Coagulopathy; fall in clotting factors II,VII, IX & X
  2. Hepatic Encephalopathy - liver flap (asterixes - flapping tremor with wrist extended) & confusion/coma
  3. Hypoalbuminaemia resulting in oedema
  4. Portal Hypertension, Oesophageal Varices and Variceal Bleeding
  5. Ascites and Spontaneous Bacterial Peritonitis (SBP)
  6. Hepatocellular carcinoma (HCC)
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25
Q

Approximately what percentage of blood flow to the liver is provided by the portal vein?

A

75%.

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26
Q

What forms the portal vein?

A

Portal vein is formed by the union of the superior mesenteric and splenic
veins and delivers blood to the liver.

27
Q

Give the 3 categories of the causes for portal hypertension.

A

Classified according to the site of obstruction:

  1. Pre-hepatic; blockage of the hepatic portal vein before the liver
  2. Intra-hepatic; distortion of the liver architecture, either pre-sinusoidal (e.g.
    schistosomiasis) or post-sinusoidal (e.g. cirrhosis)
  3. Post-hepatic; venous blockage outside the liver (RARE)
28
Q

Give a pre-hepatic cause of portal hypertension.

A

Pre-hepatic:
* Thrombosis in portal or splenic vein

29
Q

Give 2 intra-hepatic causes of portal hypertension.

A

Intra-hepatic:
* Cirrhosis (commonest cause in UK)
* Schistosomiasis (commonest cause worldwide)
* Sarcoid
* Congenital hepatic fibrosis

30
Q

Give 2 post-hepatic causes of portal hypertension.

A

Post-hepatic:
* Budd-Chiari syndrome (hepatic vein obstruction by tumour
or thrombosis)
* Right heart failure
* Constrictive pericarditis

31
Q

Explain pathophysiology of portal hypertension as a result of liver cirrhosis.

A
  1. Cirrhosis
  2. Liver injury
  3. Activated myofibroblasts contract (mediated by endothelin, NO and prostaglandins)
  4. Increased resistance to blood flow
  5. Increased back-pressure into the portal system
  6. Results in portal hypertension
32
Q

Give 4 signs for portal hypertension.

A
  1. GI bleeding - most life threatening complication
  2. Ascites
  3. Jaundice
  4. Periumbilical caput medusae
  5. Signs + symptoms of encephalopathy
33
Q

What is the mnemonic for the features of portal hypertension?

A

A - Ascites
B - Bleeding (haematemesis, piles)
C - Caput medusae
D - Diminished liver
E - Enlarged spleen

34
Q

What can portal hypertension lead to?

A

Oesophageal varices

A varices is just a dilated vein which is at risk of rupture, resulting in haemorrhage and in the GI system, it can result in GI bleeding.

35
Q

Explain the pathophysiology of oesophago-gastric varices.

A
  1. Obstruction to portal blood flow
  2. Results in portal hypertension
  3. Splanchnic vasodilation → drop in BP
  4. Increased cardiac output to compensate for BP
  5. Salt and water retention to increase blood volume and compensate
  6. Hyperdynamic circulation (high circulatory volume)/increased portal flow
  7. Formation of collaterals between the portal and systemic systems
    e.g. in the lower oesophagus and gastric cardia
  8. Gastro-oesophageal varices develop once portal pressure is above 10mmHg
  9. They start to bleed I.E. rupture when above 12mmHg - this can occur RAPIDLY and could result in MAJOR HAEMORRHAGE.
36
Q

Give 3 sites in the GI system where varices can occur.

A

They occur at the:

  1. Gastro oesophageal junction
  2. Ileocaecal junction
  3. Rectum
  4. Anterior abdominal wall via the umbilical vein (caput medusae)
37
Q

What are the potential consequences of varices?

A

If they rupture -> haemorrhage.

38
Q

Why is there the risk of rupturing for varices?

A

These vessels are thin and not meant to transport higher pressure blood, so they can easily rupture.

39
Q

Above what pressure do oesophageal varices rupture usually?

A

> 12mmHg

40
Q

What investigation can be used for oesophageal varices?

A

Investigate with upper GI endoscopy

41
Q

Treatment for stable varices.

A

1.Selective beta blocker - Propranolol
- reduces portal hypertension

  1. Endoscopic therapy - Elastic band ligation of varices
  2. Injection of sclerosant (less effective than band ligation)
42
Q

What method can be used if medical and endoscopic treatment of varices fail or if there are bleeding varices that cannot be controlled in other ways?

A

Transjugular Intra-hepatic Portosystemic Shunt (TIPS)

43
Q

Treatment for bleeding/ruptured oesophageal varices.

A

Resuscitation
1. Vasopressin analogues (I.E. terlipressin)
- Cause vasoconstriction and slow bleeding in varices
2. Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors)
3. Giving prophylactic broad-spectrum antibiotics has been shown to reduce mortality
4. Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell

Urgent endoscopy
5. Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
6. Endoscopic therapy - Elastic band ligation of varices

44
Q

What alternative method can be used in the treatment of ruptured varices if endoscopic banding fails?

A

Balloon tamponade
- To reduce bleeding by placing pressure on varices if banding fails

45
Q

What is ascites?

A

The accumulation of free fluid within the peritoneal cavity

46
Q

What type of ascites can cirrhosis cause?

A

Transudative cirrhosis
- Meaning low-protein content ascites.

47
Q

Explain why ascites can happen due to cirrhosis.

A

Low flow:
- Fluid cannot move forwards through system e.g. due to a clot
- Increased pressure in the portal system
- Causing fluid to leak out of the capillaries in the liver and into the peritoneal cavity
- Drop in circulating volume = drop in blood pressure
- Lower BP entering the kidneys and they sense this lower pressure
- Kidneys release renin
- Increased aldosterone secretion via RAAS
- Reabsorption of fluid + sodium in the kidneys

48
Q

if a cirrhosis patient presented with ascites, how would you treat this?

A
  1. Bed rest
  2. Fluid and salt restriction - low sodium diet
  3. Spironolactone ± furosemide
  4. Paracentesis (ascitic tap or ascitic drain)
  5. Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
  6. Consider TIPS procedure in refractory ascites
  7. Consider transplantation in refractory ascites
49
Q

What is the commonest serious infection in those with cirrhosis?

A

Spontaneous bacterial peritonitis.

It can also affect immunocompromised people and those undergoing peritoneal dialysis.

50
Q

What is spontaneous bacterial peritonitis (SBP)?

A

Involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation).

51
Q

Name a bacteria that can cause spontaneous bacterial peritonitis.

A

Most common organisms:

  1. Escherichia coli
  2. Klebsiella pnuemoniae
  3. Gram positive cocci (such as staphylococcus and enterococcus)
52
Q

Describe the presentation of SBP.

A
  • Can be asymptomatic so have a low threshold for ascitic fluid culture
  • Fever/Temperature
  • Abdominal pain
  • Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
  • Ileus
  • Hypotension
53
Q

Give 3 symptoms of spontaneous bacterial peritonitis.

A
  1. Dull to percussion.
  2. Temperature.
  3. Abdominal pain.
54
Q

Diagnosis for SBP.

A

Diagnosis is an ascitic tap and blood cultures

55
Q

How can SBP be diagnosed?

A

By looking for the presence of neutrophils in ascitic fluid.

56
Q

What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important.

A

It is important to do an ascitic tap so you can rule out spontaneous bacterial peritonitis as soon as possible.

57
Q

What is the management for SBP?

A
  1. ABC (airways, breathing, circulation)
  2. Treat underlying cause and treat early
  3. Insertion of nasogastric tube
  4. IV fluids
  5. Broad spectrum antibiotics - IV cephalosporin antibiotics e.g. cefotaxime, metronidazole
    - Take an ascitic culture prior to giving antibiotics
58
Q

Why is hepatorenal syndrome a complication of liver cirrhosis?

A
  • Fluid cannot move forwards through system
  • Increased pressure in the portal system
  • Causing fluid to leak out of the capillaries in the liver and into the peritoneal cavity
  • Drop in circulating volume = drop in blood pressure
  • Lower BP entering the kidneys and they sense this lower pressure
  • Kidneys release renin
  • Increased aldosterone secretion via RAAS
  • Reabsorption of fluid + sodium in the kidneys
  • Causes renal vasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney
  • Leads to rapid deteriorating kidney function

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

59
Q

Why may hepatic encephalopathy occur in cirrhosis patients?

A

There are 2 reasons that ammonia builds up in the blood in patients with cirrhosis.

Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products.

Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.

60
Q

Explain the pathophysiology of hepatic encephalopathy.

A

A major complication of liver failure:
Liver fails - nitrogenous waste (ammonia) builds up in circulation - liver can’t get rid of it - ammonia crosses the BBB and passes into brain - astrocytes clear it by converting glutamate to glutamine - excess glutamine causes an osmotic imbalance - cerebral oedema

61
Q

Give 3 signs of hepatic encephalopathy.

A

Hepatic encephalopathy
- Altered mood / dyspraxia
- Liver flap / Asterixis (flapping tremor)
- Drowsiness / confusion

62
Q

Give 4 precipitating factors for hepatic encephalopathy.

A

Precipitating Factors:

  • Constipation
  • Electrolyte disturbance
  • Infection
  • GI bleed
  • High protein diet
  • Medications (particularly sedative medications)
63
Q

Management of hepatic encephalopathy.

A
  1. Laxatives (i.e. lactulose)
    - Clear the ammonia from the gut before its absorption
    - The aim is 2-3 soft motions daily.
    - They may require enemas initially.
  2. Antibiotics (i.e. rifaximin)
    - Reduce the number of bacteria in the gut producing ammonia.
    - Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
  3. Nutritional support. They may need nasogastric feeding.
64
Q

What is peritonitis?

A

Inflammation of the peritoneum often due to infection.

8. Liver & Co (18 decks)

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