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Gastroenterology > Liver Disorders > Flashcards

Liver Disorders Flashcards

1
Q

What is the lifespan of Red blood cells?

A

120 days

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2
Q

What is the breakdown components of Haemoglobin? (3)

A
  1. Globin -> amino acids
  2. Haem -> iron + protoporphyrin
  3. Protoporphorin -> converted into unconjugated bilirubin (lipid soluble)
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3
Q

Describe the process of bilirubin production from Haemoglobin? (5)

A
  1. Haem -> iron + protoporphyrin
  2. Protoporphorin -> converted into unconjugated bilirubin (lipid soluble)
  3. Albumin binds to unconjugated bilirubin and transports it to the Liver
  4. Hepatocytes conjugate UCB to produce conjugated bilirubin which is now water soluble
  5. This is then secreted via the bile ducts and stored in the Gall bladder as a component of bile.
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4
Q

What are the steps following Bilirubin secretion from the Gallbladder? (4)

A
  1. Gall bladder secretes bile into the duodenum to help with food digestion
  2. Bacteria in the intestine convert Bilirubin —> Urobilinogen
    Urobilinogen;
  3. Some gets reabsorbed by the blood, reaching the kidneys and excreted into the urine - giving it a yellow colour
  4. Remaining urobilinogen —> further converted —> stercobilinogen which remains in the colon and excreted into the faeces giving it a distinct brown colour
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5
Q

What is the pathophysiology of Jaundice?

A
  1. Disruption of hepatocytes preventing conjugation of the bilirubin
  2. Bilirubin leaks out of the cells
  3. Eventually enter the blood stream,
  4. Leading to a yellowing of the skin and sclera - which is high in elastin and binds to bilirubin with a higher affinity, thus can be the earliest sign.
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6
Q

What is the pathophysiology of neonatal jaundice?

A
  1. High rate destruction of fetal red blood cells at birth
  2. Leads to high level of unconjugated bilirubin
  3. New born livers also have a lower amount of UGT enzyme to convert and conjugate bilirubin
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7
Q

Neonatal jaundice : complications

A

Kernicterus - unconjugated bilirubin builds up its the basal ganglia leading to brain damage

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8
Q

Neonatal jaundice : Management

A

** Phototherapy **- targets bilirubin molecules and causes them to change shape, making them more soluble and able to be excreted in the urine

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9
Q

Jaundice : Causes in children

A
  1. Haemolytic anaemia or ineffective haemopeisis
    - High volume of RBC degradation thus high levels conjugated bilirubin and aunconjugated bilirubin as hepatocytes may not be able to conjugate at this capacity
  2. Gilbert’s syndrome - low levels of UGT enzyme activity, thus process of conjugation is much slower
    - Unable to respond to physiological stress such as infection, increased hemolysis leading to a build up of Unconjugated bilirubin and jaundice.
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10
Q

What feature indicates high levels of unconjugated bilirubin in the blood?

A

**Pale urine **
* Uncojugated bilirubin cannot be excreted by the kidneys as it is not water soluble

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11
Q

Describe the anatomy of the Hepatic portal system? (5)

A
  1. Superior mesenteric vein + Inferior mesenteric vein : venous blood from small and large intestine
  2. Splenic vein : venous blood from spleen
  3. Right + Left gastric vein : venous blood from stomach
  4. Combine to form } Hepatic portal vein which contains all the nutrients absorbed from the GI tract and toxins for breakdown by liver and excretion from the kidneys
  5. Hepatic portal vein; enters the liver to form -
  6. Right and Left hepatic veins } enter the Inferior vena cave
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12
Q

Portal hypertension : Pathophysiology of disease

A
  1. Increased blood pressure in the hepatic portal venous system - largely due to hepatic cirrhosis which is when the liver tissue is replaced by fibrotic tissue.
  2. Blood is diverted from the liver - diminished liver function, decreased blood detoxification leads to a build up of toxic metabolites like ammonia.
  3. This can enter the blood stream and causes hepatic encephalopathy.
  4. Blood gets backed up into the systemic veins
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13
Q

Portal Hypertension : Clinical features (3)

A

Portal vein hypertension may be asymptomatic until complications occurs
1. Ascites, Caput medusa
1. GI bleeding 2nd to oesophageal varices
1. Jaundice if 2nd to liver dysfunction

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14
Q

Portal hypertension : Prehepatic causes

A
  • Portal vein thrombosis
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15
Q

Portal hypertension : Hepatic causes

A
  • Liver cirrhosis
  • Sarcoidosis : granulomas develop inside the liver
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16
Q

Portal hypertension : Posthepatic causes

A
  • Right sided heart failure, constrictive pericarditis : restrict the blood flow from the heart to lungs, causing blood to accumulate downwards including into the portal circulation
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17
Q

Portal hypertension : Investigations for diagnosis

A
  1. Gold standard - measure of a hepatic venous pressure gradient, Liver US,
  2. CT scan or MRI, Endoscopy - reveals varices.
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18
Q

Portal hypertension : Management

A
  1. TIPS procedure - intrahepatic protosystemic shunt to decrease hepatic portal pressure and prevent complications
  2. Betablockers e.g Propanolol - decreases portal venous pressure
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19
Q

Portal Hypertension : Complications

A
  1. Oesophageal varices
  2. Haeorrhoids
  3. Hypersplenism
  4. Ascites
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20
Q

Variceal haemorrhage : management

A
  1. Resuscitation :Blood + clotting agent transfusion, IV fluid resus
  2. Vasoactive agent : Telipressin for haemostats and rebreeding
  3. Prophylactic antibiotics in liver cirrhosis (reduced mortality)
  4. Endoscopy;
    First line : Band ligation
    Second line: Sengstaken-Blakemore tube
    Third line : TIPPS procedure
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21
Q

ALT enzyme : Where is it found?

A
  1. Origin : found in high concentrations in the liver.
  2. ALT is usually higher than AST in most types of liver disease in which the activity of both enzymes is predominantly from the hepatocyte cytosol.
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22
Q

AST enzyme : origin?

A
  1. Origin : found in the liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leucocytes, and red cells.
  2. It is not as sensitive or specific for the liver as ALT and elevation in AST may be seen as secondary to nonhepatic causes as well.
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23
Q

ALT : Causes of elevation?

A
  1. Acute or chronic viral hepatitis
  2. Steatohepatitis
  3. acute Budd-Chiari syndrome,
  4. ischemic hepatitis,
  5. autoimmune, hemochromatosis, medications/toxins, alpha1-antitrypsin deficiency, Wilson disease, Celiac disease
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24
Q

Alkaline phosphatase : Origin?

A

Origin : highly concentrated in the microvilli of the bile canaliculus as well as several other tissues (e.g., bone, intestines, and placenta)

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25
Q

GGT : Origin?

A

Origin : on membranes of cells with high secretory or absorptive activities.

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26
Q

GGT : significance of rise?

A
  • More specific for biliary disease when compared to alkaline phosphatase because it is not present in bone
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27
Q

Liver enzymes : Cholestatic pattern?

A
  • Cholestatic pattern : indicates osbtruction of the biliary tract
  • Elevated alkaline phosphatase + gamma glutamyl transferase + bilirubin > out of proportion to AST and ALT
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28
Q

Whta is cholestatic disease?

A
  • Disorder chracterised by impaired bile flow within the liver or from the liver to the small intestine
  • Distruption normal flow of bile
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29
Q

ALP + GGT + Bilirubin > AST and ALT : Hepatobiliary causes

A
  1. Bile duct obstruction
  2. primary biliary cirrhosis,
  3. primary sclerosing cholangitis
  4. infiltrating diseases of the liver (sarcoidosis, amyloidosis, lymphoma, among others), cystic fibrosis, hepatic metastasis, cholestasis
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30
Q

ALP + GGT + Bilirubin > AST and ALT : Non hepatic causes?

A
  1. Bone disease,
  2. Pregnancy,
  3. Chronic renal failure
  4. .Lymphoma or other malignancies, congestive heart failure, childhood growth, infection, or inflammation
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31
Q

Liver Cirrhosis : Pathophysiology of disease (5)

A
  1. Repeated insult to the liver due to excess alcohol or toxins can cause fibrosis
    - process mediated by stellate checks that sit between the sinusoid and hepatocytes known as the pre sinusoidal space.
  2. Stellate cells main function is to store vitamin A
  3. Hepatocytes damage causes them to release paracrine factors which activates changes in stellate cells.
  4. Stellate cells lose vitamin A, and secrete growth factor which causes them to produce collagen resulting in fibrosis
  5. Fibrotic tissue starts to build up and compress the central veins and sinusoids - resulting in Portal vein hypertension.
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32
Q

Liver cirrhosis : complications (5)

A
  1. Inability to metabolise and break down oestrogen : high levels of oestrogen in the blood can lead to gynecosmastia
  2. Inability to conjugate bilirubin : increase level of unconjugated bilirubin in the blood, leads to jaundice
  3. Inability to produce proteins : hypoalbuminaemia
  4. Inability to produce coagulation factors : coagulopathy
  5. Hepatic encephalopathy - release of toxins and ammonia in the blood.
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33
Q

Liver cirrhosis : Scoring system

A
  1. Model for end stage liver disease (MELD) - ( Child-Pugh classification was previously used)
  2. Used to assess severity of liver cirrhosis particularly for patients on list for liver transplant
  3. MELD - combination of bilirubin, creatinine and INR used to calculate 3 month mortality likelihood.
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34
Q

Liver cirrhosis : Investigation for diagnosis

A

Fibroscan - transient elastography a type of US to measure stiffness of the liver

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35
Q

Liver cirrhosis : Who should be offered screening and what does it entail?

A

** NICE Recommendations for :**
1. Upper endoscopy to check for varices in newly dx liver cirrhosis
2. Liver US every 6 months +/- alpha-feta protein to check for hepatocellular cancer

Screening should be offered to;
1. People with hepatitis C infection
2. Hx of severe alcohol excess
3. Alcoholic liver disease

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36
Q

Liver cirrhosis : Lab results?

A
  1. Elevated bilirubin
  2. Elevated liver enzymes
  3. Low platelet count
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37
Q

Acute liver failure : Definition

A
  1. Rapid onset of heaptocellular dysfunction leading to a variety of systemic complications
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38
Q

Acute Liver failure : Causes

A
  1. Paracetamol overdose
  2. Alcohol
  3. Viram hepatitis (A or B)
  4. Acute fatty liver of pregnancy
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39
Q

Acute Liver failure : Clinical features

A
  1. Jaundice
  2. Coagulopathy
  3. Hypoalbunaemia
  4. Hepatic encephalopathy
  5. Renal failure - hepatorenal syndrome
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40
Q

Liver disease : Explain the coaagulopathy seen?

A

Increases risk of thrombosis AND risk of bleeding

  1. In liver disease - all clotting factors are low except for ‘Factor VIII’
  2. Factor VIII - synthesis in the endothelial cells through out the body and not exclusively by the hepatocytes
  3. Poor function of the Liver - Factor VIII is nor cleared from the blood stream by the liver
  4. Higher levels of circulation Factor VIII, increases risk of thrombosis.
  5. Also - poor hepatic function reduces synthesis of anticoagulants such as Protein C, Protein S and anti-thrombin : increased risk of thrombosis
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41
Q

Non alcoholic fatty liver disease : Definition

A
  • Fat deposition in the liver which is unrelated to alcohol or viral causes
  • Associated with metabolic syndrome - obesity, diabetes, high cholesterol and hyperlipidaemia
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42
Q

Non alcoholic fatty liver disease : Pathophysiology

A
  1. Insulin resistance develops in various tissues including the liver
  2. Reduced response to insulin by the liver causes it to increase fat storage and decrease fatty acid oxidation.
  3. This results in decreased secretion of lipids into the blood and increased uptake of fatty acids from the blood, in a process called steatosis.
  4. Fat droplets form within the hepatocytes, resulting in inflammation - known as steatohepatitis.
  5. The chronic seato-hepatitis causes the stellate cells to lay down fibrotic tissue resulting in fibrosis.
  6. Chronic inflammation can cause fibrosis to progress into cirrhosis.
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43
Q

Non alcoholic fatty liver disease : Investigations for diagnosis

A
  1. US liver : Hepatomegaly and increased echogenicity
  2. Liver biopsy : to confirm the diagnosis
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44
Q

What is the management if an incidental finding of NAFLD?

A

ELF - Enhanced liver fibrosis test : blood test to check for advanced fibrosis

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45
Q

Non alcoholic fatty liver disease : Lab results of liver enzymes

A

Destruction of hepatocytes lead to release of liver enzyme into the blood;
* ALT (alanine transaminase) levels > AST (aspartate transaminase) of > 2

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46
Q

Alcoholic liver disease : Pathophysiology

A
  1. Ethanol —> (enzyme alcohol dehydrogenase) —> acetaldehyde
    NAD+ —> NADH
  2. High NADH and low NAD+ levels stimulate hepatocytes to produce more fatty acids, resulting in steatosis.
  3. Acetaldehyde can bind to molecules and proteins within the liver - forming acetaldehyde adducts which are recognised by the immune system as a foreign bodies, causing inflammation.
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47
Q

What is the disease progress in Alcoholic Liver disease?

A

Alcoholic fatty liver disease —> alcoholic hepatitis —> Alcoholic cirrhosis

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48
Q

Alcoholic liver disease : Investigation for diagnosis

A

Histology on biopsy : In Alcoholic hepatitis, mallory bodies which are damaged filaments of proteins are found in the histology.

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49
Q

Alcoholic liver disease : Labs result of liver enzymes

A

Liver enzymes : AST:ALT > ratio of 3, Gamma-GT is elevated

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50
Q

Alcoholic liver disease : Management

A
  1. Life style advice - avoid excess alcohol consumption
  2. Glucocorticoids e.g. Prednisolone - use to suppress immune system in the management of acute episode of alcoholic hepatitis
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51
Q

Hepatitis : Definition

A

Inflammation of the liver secondary to a virus

52
Q

Hepatitis : Pathophysiology

A
  1. Viruses target hepatocytes causing them to display their antigens on the MHC class 1 molecules
  2. Triggers immune cell to infiltrate the liver and cause destruction of the infected hepaocytes
  3. Cytoxic destruction of the hepatocytes causes liver inflammation and hence hepatitis
53
Q

Hepatitis : Clinical features

A
  1. Fever, malaise, nausea
  2. Hepatomegaly
  3. Hepatocyte damage - release of a mix of both conjugated and unconjugated bilirubin into the bloodstream
    -Dark urine : due to rise in urobiinogen and conjugated bilirubin leaking into the blood and entering the urine
54
Q

Hepatitis : Lab results of LFTs

A

Labs : raised ALT, raised AST, raised WCC

55
Q

Heptatitis A : transmission and presentation

A

Transmission : through ingestion of contaminated food and water.
Presentation : Only presents as an acute episode - not chronic.

56
Q

Heptatitis A : Lab results?

A

HAV-IgM antibody : indicates active infection
HAV-IgG : indicates previous infection or vaccination

57
Q

Hepatitis A : Management

A

Option for immunisation

58
Q

Heptatitis E: transmission and presentation

A

Transmission : trasmitted via oral-fecal route, acquired through undercooked sea food or contaminated water
Presentation : Only presents as an acute episode - not chronic.

Can be very serious in pregnant women

59
Q

Hepatitis E : Lab results?

A

HEV-IgM antibody : indicates active infection
HEV- IgG : indicates previous infection or vaccination

60
Q

Hepatitis E : Management

A

No option for immunisation

61
Q

Heptatitis C : Transmission and presentation

A

Transmission : mostly via blood but low chance also via bodily fluids through sex e.g. IVDU,transfusion, childbirth, sex

Presentation : Can develop into chronic hepatitis

62
Q

Heptatitis C : Lab results

A

HCV-IgG - is not regarded as a protective antibodies
HCV RNA test (gold standard) -can detect it within 1-2 weeks

63
Q

Heptatitis B: Transmission and presentation

A

Transmission :mostly via sex/exchange of bodily fluids and blood
Presentation : develop into chronic hep B in 20% of cases, chronic Hep B is known to be linked to liver cancer.

64
Q

What is the main complication of Hepatitis B?

A

Chronic Hepatitis B can develop into Hepatocellular cancer

65
Q

Hepatitis B : HBsAg (HBV surface antigen)?

A

Key marker for HBV infection, present in acute infection then cleared in recovery.
If present for >6 months this indicates a chronic infection

66
Q

Hepatitis B : HBcAg (HBV core antigen)

A
  1. Antigens from the core of the virus, present in active infection for 6 months, if present longer, individual is a carrier
67
Q

Hepatitis B : Anti- HBe

A

Anti- HBe - secreted by infected cell ad marker of active viral replication, indicates active infection

68
Q

Hepatitis B : Anti- HBs

A

Implies immunity either through exposure or immunisation

69
Q

Hepatitis B : Anti- HBc

A

Anti-HBc - implies previous or current infection
* IgM anti-HBc : appears during acute or recent hepatitis B infection and is present for around 6 months
* IgG anti-HBc : persists following infection >6 months ago

70
Q

Hepatitis B : In pregnancy?

A
  1. If pregnancy with Hep B - given vaccination + Hep B immunoglobulin
  2. Cannot be transmitted via breastfeeding (unlike HIV)
71
Q

Primary biliary cirrhosis/cholangitis : Pathophysiology (4)

A
  1. Immune reaction, antibodies are created against the mitochondria of the cells within the bile ducts.
  2. Autoimmune disease where T cells attack the cells that line the smaller sized bile ducts in the liver
  3. As cells are damaged by immune attack, they start letting bile leaking into the hepatocytes and the blood.
  4. Inflammation of the bile ducts results in cholangitis, can cause progressive cholestasis, over time chronic inflammation can result in cirrhosis.
72
Q

Primary biliary cirrhosis/cholangitis : Which other diseases is it associated with?

A

Associated with other immune disorders;
* Sjoren’s syndrome (seen in 80% of patients)
* Rheumatoid arthritis
* Systemic sclerosis

73
Q

Primary biliary cirrhosis/cholangitis : Clinical feature

A
  1. Pruritus and itching - due to bile salts
  2. Cholestatic jaundice - bile and conjugated bilirubin leaking into the blood
  3. Xanthomas, xanthelasmas: Cholesterol within the bile - deposits within the skin,
  4. RUW, Hepatomegaly - can lead to liver failure
  5. Sx of sjoren’s syndrome and rheumatoid arthritis
74
Q

Primary biliary cirrhosis/cholangitis

A

Itching in middle aged women

75
Q

Primary biliary cirrhosis/cholangitis : Demographic

A
  1. Middle aged females 9:1
76
Q

Primary biliary cirrhosis/cholangitis : Investigations for diagnosis (blood tests and imaging results)

A
  1. Immunology;
    * Anti-mitochondrial (AMA) antibodies present in 98% of patients
    * Raised IgM antibodies
    Imaging
  2. Ultrasound or MRCP of the liver/biliary tract to exlcude extrahepatic biliary obstruction
77
Q

Autoimmune hepatitis : definition

A

Chronic inflammatory liver disease where antibodies are produced against hepatocytes

Unknown etiliology

78
Q

Autoimmune hepatitis : Epidemiology

A
  1. Young females
  2. Associated with HLA-DR3 and HLA-DR4 which are both MHC class II surface receptors.
79
Q

Autoimmune hepatitis (Type 1) : Which antibodies are found?

A

Type 1 - 80% of autoimmune hepatitis cases
* Anti-nuclear antibodies (ANA present)
* Anti-smooth muscle antibodies (ASMA present)

80
Q

Autoimmune hepatitis (Type 2) : Which antibodies are found?

A

Type 2 - 20%
Defined as presence of antibodies to microsomes of the kidney or liver
1. Anti-liver/kidney microsomal antibody (ALKM antibody)

81
Q

Autoimmune hepatitis : Clinicall features

A
  1. Amenorrhea (common)
  2. Acute/Chronic liver disease } jaundice, fever
82
Q

Autoimmune hepatitis : Management

A
  1. Steroids and immunosuppressants e.g. Azathiprine
  2. Liver transplantation
83
Q

Primary sclerosis cholangitis : Definition

A
  1. Sclerosis refers to hardening of tissues and cholangitis is the inflammation of the bile ducts
  2. Fibrosis and inflammation of both the intrahepatic and extra hepatic ducts
84
Q

Primary sclerosis cholangitis :Pathophysiology

A

Autoimmune disease attacking and destroying the bile ducts epithelial cells - link with HLA B8 and HLA-DR3.

85
Q

Primary sclerosis cholangitis : Which other diseases is it associated with?

A

Ulcerative colitis (80% of patient)
Crohns

86
Q

Primary sclerosis cholangitis : Main complication?

A

Risk of cholangiocarcinoma

87
Q

Primary sclerosis cholangitis : Clinical features

A
  1. Fibrosis obstructs the flow of bile, thus sx of obstructive jaundice
  2. Pruritus - bile salts and acids deposit in the skin\
  3. Jaundice
    -Dark urine - conjugated bilirubin is filtered out via the kidneys
    RUQ pain
88
Q

Primary sclerosis cholangitis : Investigations for diagnosis

A
  1. ERCP/MRCP - Gold standard with biosy may show ‘onion skin’
89
Q

Primary sclerosis cholangitis : Lab results?

A

Immunology;
1. Perinuclear anti-neutrophil cytoplasmic antibody (pANCA positive)
2. Elevated IgM

Lab results;
1. Raised bilirubin - bilirubinuria
2. Raised ALP and GGT

90
Q

Primary sclerosis cholangitis : Management

A

Immunosupression

91
Q

What are the differences between Primary Biliary Cholangitis and Primary Sclerosing cholangitis?

A

Primary biliary cholangitis
* - Associated with autoimmune disorder
* - Primarily affects the small bile ducts in the liver and causes accumuation of bile in the liver
* - Most common in middle afed wineb

Primary sclerosing cholangitis
* Immune and genetic factors - associated with Ulcerative colitis
* Characterised by inflammation and scarring inside and outside of the liver - can cause strictures and also affects larger bile ducts
* More common in younger men

92
Q

Name the drugs which may induce/contribute to Liver damage and disease?

A
  1. Paracetamol
  2. Anti-epileptics : Sodium valproate, phenytoin
  3. Psychiatric drugs : Methyldopa
  4. Tuberculosis drugs : Isoniazid, rifampicin, pyrazinamide
  5. Statins
  6. Alcohol
93
Q

Name the drugs which can cholestasis +/- hepatitis?

A
  1. Combine oral contraceptives - increases risk of gall stones forming
  2. Antibiotics - Flucloxacillin,** co amoxiclav**
  3. Phenothiazine - prochlorperazine
  4. Sulphonylureas
94
Q

Name the drugs which can cause Liver Cirrhosis?

A
  1. Methotrexate
  2. Methyldopa
  3. Amiodorone
95
Q

Cholangiocarinoma : Definition?

A
  1. Rare cancer of the bile duct arising from the epithelial cells of the intrahepatic and extra hepatic bile ducts
  2. High fatality due to late diagnosis and highly proliferative
96
Q

Cholangiocarinoma : Risk factors?

A
  1. Primary sclerosis cholangitis (main risk factor),
  2. Chronic liver disease such as hepatitis or cirrhosis,
  3. Obesity
97
Q

Cholangiocarcinoma : Clinical symptoms (3)

A
  1. Systemic : general malaise, weight loss, abdominal pain
  2. Extra hepatic disease - obstruction of drainage of bile from the liver
    Jaundice, pruritus, dark urine
  3. Intra hepatic disease : dull RUQ pain, malaise, weight loss
98
Q

Cholangiocarcinoma : Clinical signs

A
  1. ‘Courvoisier sign’ - palpable mass in the RUQ
  2. ‘Sister Mary Joseph nodes’ - periumbilical lymphadenopathy
99
Q

Cholangiocarcinoma : Investigations for diagnosis

A

Abdominal US with biopsy

100
Q

Cholangiocarcinoma : Tumor marker

A

Tumor markers : CA 19-9, CEA

101
Q

Cholangiocarcinoma : Lab results

A

Raised LFTs : elevated GGT, ALP
Elevated bilirubin

102
Q

Cholangiocarcinoma : Management

A

Surgery for resection + chemotherapy

103
Q

Ascities : Definition

A

abnormal accumulation of fluid in the abdomen

104
Q

Ascites : What are the two categories?

A
  1. Serum ascites albumin level >11g/L
    -normal level of protein in the blood, fluid in the abdomen is due to fluid load
  2. Serum ascites albumin level <11g/L Due to low protein in the blood,
    - reduced oncotic pressure
    - Hypoalbunaemia - Nephrotic syndrome, severe malnourishment
105
Q

Ascites : Causes of serum ascites albumin level <11g/L

A
  1. Hypoalbunaemia - Nephrotic syndrome, severe malnourishment
  2. Infections - tuberculosis
  3. Other - pancreatitis, bowel obstruction, biliary ascites
106
Q

Ascites : Causes of serum ascites albumin level >11g/L

A
  1. Liver disorders e.g. cirrhosis, acute liver failure, liver metastases
  2. Cardiac disorders e.g. Right heart failure, constrictive pericarditis
  3. Other : Budd-Chiari syndrome, Portal vein thrombosis
107
Q

Ascites : Management

A
  1. Reduce dietary sodium
  2. Fluid restriction if sodium <125
  3. Aldosterone antagonists e.g. Spirnolactone to reduce sodium- can add loop diuretics if not sufficient response
  4. Prophylactic antibiotics - reduce risk of spontaneous bacterial peritonitis
  5. Abdominal paracentesis - for large volume ascites
108
Q

Ascites : Guidelines for Abdominal paracentesis

A
  1. Albumin cover : as removal of large volume of fluid >5L is associated with high rate of ascites recurrent, development of hepatorenal syndrome and higher rates of mortality
109
Q

Spontaneous bacteria peritonitis : Definition

A

Bacterial infection of the peritoneal cavity of the abdomen

Commonly seen in patient sight ascites 2nd to liver cirrhosis
If due to Alcoholic liver disease - poor prognosis

110
Q

Spontaneous bacteria peritonitis : Clinical features

A

Abdominal pain and tenderness,
Fever
Worsening ascite

111
Q

Spontaneous bacteria peritonitis : Investigations for diagnosis

A

Paracentesis - neutrophil count >250 cells,
-most common organism is E.coli

112
Q

Spontaneous bacteria peritonitis : Management

A

IV Ceforaxime

113
Q

Spontaneous bacteria peritonitis : When are prophylactic antibiotics indicated and which?

A

Prophylactic Abx (Ciprofloxacin) should be given after ascites resolves if;
1. previous episode of SBP, Fluid protein <15
2. Child-Pugh of 9<
3. Hepatorenal syndrome

114
Q

Primary Hepatocellular carcinoma : Pathophysiology (2)

A
  1. Mutation of the hepatocytes, observed when liver cells are forced to repair at a high frequency,
  2. This can be caused by any diseases which leads to cirrhosis and scarring of the liver tissue such as alcoholic hepatitis etc.
115
Q

What is the most common cause of heaptocellular carcinoma
- In the world?
- In the UK?

A
  1. World :Chronic hepatits B
  2. Europe : Chronic hepatits C
116
Q

Primary Hepatocellular carcinoma : Risk factors

A
  1. Heptitis B and C
  2. Alcohol
  3. Hemochromatosis
  4. Primary billiary cirrhosis
117
Q

Primary Hepatocellular carcinoma : Tumor marker

A

Alpha feta protein tumor marker - raised as can be produced by the tutor or proliferating cells

118
Q

Hepatocellular carcinoma : Clinical features

A

Symptoms present late
General sx of liver cirrhosis and liver failure:
1. RUQ pain
2. Hepatosplenomegaly
3. Pruritus
4. Ascites

119
Q

Primary Hepatocellular carcinoma : 2WW criteria

A

If upper abdominal mass consistent with enlarged liver : 2WW Ultrasound scan

120
Q

Primary Hepatocellular carcinoma : Lab results

A

Labs;
1. Destruction of hepatocytes - raised ALP and GGT
2. Alpha feta protein tumor marker

121
Q

Primary Hepatocellular carcinoma : Screening protocol

A

Screening with US +/- alpha-fetoprotein for high risk groups such as ;
* Patients with liver cirrhosis 2nd to Hep B/C
* haemochromatosis
* alcohol abuse

122
Q

Primary Hepatocellular carcinoma : Management

A
  1. Surgical resection with chemotherapy
  2. Radiofrequency ablation
  3. Liver transplantation
123
Q

Hepatorenal syndrome ; Definiton

A
  1. Serious and potentially life-threatening complication of advanced liver disease, particularly cirrhosis.
  2. Characterized by the development of acute kidney injury in individuals with severe liver dysfunction
124
Q

Hepatorenal syndrome : Pathophysiology

A
  1. Portal Hypertension and Systemic Vasodilation:
    -Liver cirrhosis causes liver scarring which increases resistance to blood flow through the liver, leading to portal hypertension.

-Portal hypertension can result in the dilation of blood vessels (vasodilation) in other parts of the body, including the kidneys.

  1. Activation of the Renin-Angiotensin-Aldosterone System (RAAS): The decreased blood flow to the kidneys due to vasodilation triggers the activation of the RAAS
  • This activation leads to increased retention of sodium and water by the kidneys, further contributing to fluid overload.
  1. Sympathetic Nervous System Activation: The sympathetic nervous system, which plays a role in the body’s “fight or flight” response, is activated in response to reduced renal perfusion.
  • This activation leads to vasoconstriction of renal blood vessels, which can exacerbate renal dysfunction.
  1. Circulatory Changes and Renal Ischemia: reduced blood flow to the kidneys lead to ischemia (inadequate blood supply), impairing the kidney function
125
Q

Hepatorenal syndrome : Clinical features

A

Signs of Kidney injury
1. Decrease in urine output, increased levels of creatinine,and electrolyte imbalances

Signs of advanced liver disease
1. Ascites (fluid accumulation in the abdomen)
1. Hepatic encephalopathy (a decline in brain function due to liver dysfunction), may also be present.

126
Q
A

Gastroenterology (5 decks)

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