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GI Pathology > 8. Jaundice and chronic liver disease > Flashcards

8. Jaundice and chronic liver disease Flashcards

1
Q

List synthetic functions of the liver.

A
  • Clotting factors
  • Bile acids
  • Carbohydrates: Gluconeogenesis, Glycogenolysis, Glycogenesis
  • Proteins: Albumin synthesis
  • Lipids: Cholesterol synthesis, Lipoprotein and TG synthesis
  • Hormones: Angiotensinogen, insulin like growth factor
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2
Q

What are other functions of the liver?

A
  1. Detoxification:
    - Urea production from ammonia
    - Detoxification of drugs
    - Bilirubin metabolism
    - Breakdown of insulin and hormones
  2. Immune function:
    - Combating infections (get rid of bacteria etc.)
    - Clearing the blood of particles and infections
    - Neutralizing and destroying all drugs and toxins
  3. Storage:
    - Stores glycogen
    - Stores Vitamin A, D, B12 and K
    - Stores copper and iron
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3
Q

What are liver function tests?

A
  • Bilirubin
  • Aminotransferases (ALT, AST)
  • Alkaline phosphatase
  • Gamma-glutamyl transpeptidase (gamma-GT)
  • Albumin
  • Prothrombin time
  • Creatine
  • Platelet count
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4
Q

Bilirubin:

  1. How is it made?
  2. What role does liver play in its metabolism?
  3. List reasons why it might be elevated?
A
  1. By product of haem metabolism. Generated by senescent RBC’s in spleen.
  2. Initially bound to albumin (unconjugated). Liver helps to solubilise it (conjugated).
  3. Elevated as a result of:
    - Pre-hepatic: Haemolysis
    - Hepatic: Parenchymal damage
    - Post hepatic: Obstructive
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5
Q

Aminotransferases:

  1. Where are they present?
  2. Name them.
  3. Why is it important to test them?
A
  1. Present in hepatocytes.
  2. Aspartate aminotransferase (AST) and Alanine aminotransferase (ALT)
  3. These enzymes are contained in hepatocytes and leak into the blood with liver cell damage.
    - AST: primarily a mitochondrial enzyme and is also present in heart, muscle, kidney and brain. High levels are seen in hepatic necrosis, myocardial infarction, muscle injury and congestive cardiac failure.
    - ALT: is a cytosol enzyme, more specific to the liver, so that a rise only occurs with liver disease.
    - ALT : AST ratio is a useful clinical indicator. In alcoholic liver disease and steatohepatitis, the AST is often greater than the ALT.
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6
Q

Alkaline phosphatase:

  1. Where is it present?
  2. When is it elevated?
A
  1. Present in hepatic canalicular (ducts) and sinusoidal membranes, and also in bone, intestine and placenta.
  2. Serum ALP is raised in both intrahepatic and extrahepatic cholestatic disease (obstruction) of any cause, due to increased synthesis.
    Raised levels also occur with hepatic infiltrations (e.g. metastases) and in cirrhosis.
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7
Q

Gamma-glutamyl transpeptidase:

  1. Is it liver specific?
  2. What elevates it levels?
  3. What is it useful in?
A
  1. Nope, also present in other tissues.
  2. Alcohol, drugs such as NSAIDs
  3. Useful to confirm liver source of ALP. In cholestasis, the γ-GT rises in parallel with the ALP.
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8
Q

Albumin:

  1. What is this marker for?
  2. Why is interpretation difficult for low levels of albumin?
A
  1. Marker of synthetic function of liver. Useful for gauging the severity of chronic liver disease: a falling serum albumin is a bad prognostic sign.
  2. Difficult when other causes of hypoalbuminaemia (e.g. malnutrition, urinary protein loss or sepsis) are present.
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9
Q

Prothrombin time (PT):

  1. What is it?
  2. Why is it important?
A
  1. PT tells you how long it takes to clot blood. High PT means liver is not making right amount of clotting factors.
  2. Extremely important test for liver function. Tells degree of liver dysfunction. Used to calculate scores to decide stage of liver disease, who needs a liver transplant and who gets a liver transplant
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10
Q

Creatinine:

  1. Which organ’s function creatinine test indicates?
  2. What’s its importance with respect to liver?
A
  1. Indicates kidneys function.

2. Determines survival from liver disease. Critical assessment for need for transplant.

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11
Q

Platelet count:

  1. Thrombopoietin is made by which organs?
  2. Why is it important to test this as part of liver function test?
A
  1. Thrombopoietin (hormone that regulates platelet production) is produced by liver and kidney.
  2. Cirrhosis results in splenomegaly. Platelets low (thrombocytopenia) in cirrhotic subjects as a result of hypersplenism. Indirect marker of portal hypertension.
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12
Q

What symptoms you might see in a patient with liver dysfunction?

A

Jaundice
Ascites
Variceal bleeding
Hepatic encephalopathy

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13
Q

Jaundice:

  1. Define it.
  2. When is it detectable?
  3. Name a differential diagnosis.
A
  1. Yellowing of the skin, sclerae, and other tissues caused by excess circulating bilirubin.
  2. Detectable when total plasma bilirubin levels exceed 34 µmol/L
  3. Differential diagnosis is carotenemia (yellow pigmentation of the skin (xanthoderma) and increased beta-carotene levels in the blood).
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14
Q
  1. What are pre-hepatic causes of jaundice?
  2. What clues you may get from history indicating pre-hepatic jaundice?
  3. What clues you may get from clinical examination indicating pre-hepatic jaundice?
A
  1. Increased quantity of bilirubin (Haemolysis)
    Impaired transport
  2. History of anaemia (fatigue, dyspnoea, chest pain)
    Acholuric jaundice (elevated unconjugated bilirubin but with no bile pigments).
  3. Pallor, Splenomegaly
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15
Q
  1. What are hepatic causes of jaundice?
  2. What clues you may get from history indicating hepatic jaundice?
  3. What clues you may get from clinical examination indicating hepatic jaundice?
A
  1. Defective uptake of bilirubin. Defective conjugation. Defective excretion
  2. Risk factors for liver disease (IVDU, drug intake)
    Decompensation (ascites, variceal bleed, encephalopathy)
  3. Stigmata of chronic liver disease (spider naevi, gynaecomastia)
    Ascites, Asterixis (tremor of the hand when the wrist is extended - bird flapping).
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16
Q
  1. What are post-hepatic causes of jaundice?
  2. What clues you may get from history indicating post-hepatic jaundice?
  3. What clues you may get from clinical examination indicating post-hepatic jaundice?
A
  1. Defective transport of bilirubin by the biliary ducts
  2. Abdominal pain
    Cholestasis (Pruritus, pale stools, high coloured urine)
  3. Palpable gall bladder (Courvoisier’s sign)
17
Q

What investigations would you carry out if liver abnormality suspected?

A
  1. Liver screen:
    - Hepatitis B & C serology
    - Autoantibody profile, serum immunoglobulins
    - Caeruloplasmin and copper
    - Ferritin and transferrin saturation
    - Alpha 1 anti trypsin (enzyme deficiency can cause cirrhosis)
    - Fasting glucose and lipid profile
  2. Most important test is Ultrasound of the abdomen:
    - Differentiates extrahepatic and intrahepatic obstruction
    - Delineates site and cause of obstruction
    - Documents evidence of portal hypertension
    - Preliminary staging of extent of disease e.g. cancer spread
18
Q

Compare use of ultrasound and CT/MRI scan.

A

US: good for gallstones.
MRI/CT: better for pancreas.
Both have high specificity but CT/MRI has better sensitivity.
Both can examine organs as well as biliary system

19
Q

Compare MRCP with ERCP.

A
  • MRCP = no radiation. ERCP = radiation
  • MRCP = no complications. ERCP = 5% complications
  • ERCP offers therapeutic options but MRCP doesn’t
  • ERCP = only image ducts
  • MRCP: some experience claustrophobia
  • ERCP requires sedation
20
Q

When are therapeutic ERCP’s used?

A
  • Dilated biliary tree ± visible stones, ± tumour
  • Acute gallstone pancreatitis
  • Stenting of biliary tract obstruction
  • Post-operative biliary complications
21
Q

Name complications associated with ERCP.

A
  1. Sedation related: respiratory, cardiovascular
  2. Procedure related:
    - Pancreatitis
    - Cholangitis
    - Sphincterotomy (A way to remove gall stones, by cutting the sphincter open and pulling the stones out the way) (Bleeding, Perforation)
22
Q
  1. When is Percutaneous Transhepatic Cholangiogram (PTC) used?
  2. Name a disadvantage of PTC used.
A
  1. Used when ERCP not possible due to duodenal obstruction or previous surgery. Used for Hilar stenting.
  2. More invasive than ERCP so high risk of infection
23
Q

When is endoscopic ultrasound used?

A

Characterising pancreatic masses
Staging of tumours
Fine needle aspirate (FNA) of tumours and cysts
Excluding biliary microcalculi

24
Q

Define chronic liver disease.

A

Liver disease that persists beyond 6 months:

  • Chronic hepatitis
  • Chronic cholestasis
  • Fibrosis and Cirrhosis
  • Others e.g. steatosis
  • Liver tumours
25
Q

What causes cirrhosis?

A
  • Alcohol
  • Autoimmune: PBC (Primary Biliary cholangitis), PSC (Primary Sclerosing Cholangitis) autoimmune hepatitis
  • Haemochromatosis
  • Chronic Viral hepatitis: B & C
  • Non-alcoholic fatty liver disease (NAFLD)
  • Drugs (MTX, amiodarone)
  • Cystic fibrosis, a1antitryptin deficiency, Wilsons disease
  • Vascular problems (Portal hypertension + liver disease)
  • Cryptogenic
  • Others: sarcoidosis, amyloid, schistosomiasis
26
Q

Outline clinical presentation of cirrhosis.

A
  1. Compensated chronic liver disease:
    - Routinely detected on screening tests
    - Abnormality of liver function tests
  2. Decompensated chronic liver disease:
    - Ascites
    - Variceal bleeding
    - Hepatic encephalopathy
  3. Hepatocellular carcinoma
27
Q

What are the clinical features of Ascites?

A
  • Physical exam reveals dullness in flanks and shifting dullness (approx 1500cc). Can be confirmed by U/S which can detect up to 100cc.
  • Corroborating evidence:
    > Spider naevi, palmar erythema, abdominal veins, fetor hepaticus
    > Umbilical nodule
    > JVP elevation
    > Flank haematoma
28
Q

How is ascites diagnosed?

A

All patients with new-onset ascites should have a diagnostic paracentesis (i.e. removal of a small quantity of fluid for testing). The fluid is tested for:

  • Protein & albumin concentration
  • Cell count and differential
  • SAAG (serum-ascites albumin gradient)
29
Q

What does SAAG show?

A

If SAAG >1.1g/dl then it indicates the ascites is due to portal hypertension, either liver related or non-liver related (97% accurate). Important causes of high SAAG ascites (> 1.1 g/dl) include: cirrhosis of the liver, heart failure, Budd-Chiari syndrome, portal vein thrombosis, and idiopathic portal fibrosis, myexdema.

If SAAG <1.1g/dl indicates causes of ascites not associated with increased portal pressure such as: tuberculosis, pancreatitis, infections, serositis, malignancy etc.

30
Q

How is ascites treated?

A 
Diuretics
Large volume paracentesis
TIPS
Aquaretics
Liver transplantation
31
Q

Variceal haemorrhage:

  1. What causes varices?
  2. where do they occur?
A
  1. Portal hypertension
  2. Occur at porto-systemic anastomoses e.g. Skin (Caput medusa), Oesophageal & Gastric, Rectal, Posterior abdominal wall, Stomal. These are medical emergencies.
32
Q

How is variceal haemorrhage managed?

A

Resuscitate patient
Good IV access
Blood transfusion as required
Emergency endoscopy (use band ligation and add Terlipressin for control. Sengstaken-Blakemore tube for uncontrolled bleeding. TIPSS for re-bleeding after banding).

33
Q

Hepatic encephalopathy:

  1. What is it?
  2. What can precipitate it?
  3. What might be clinical signs of it?
  4. Other than treating underlying cause what else can be done?
  5. When is liver transplant indicated?
A
  1. Confusion due to liver disease. Graded 1-4.
  2. GI bleed, infection, constipation, dehydration, medication esp. sedation so treating underlying cause important.
  3. asterixis (flap) and foetor hepaticus (bad smell)
  4. Laxatives (phosphate enemas and lactulose), Neomycin, Rifaximin-broad spectrum non absorbed antibiotic
  5. If repeated admissions with HE.
34
Q

What is hepatocellular carcinoma associated with?

A

Cirrhosis

Chronic hepatitis B and C

35
Q

How does hepatocellular carcinoma present?

A 
Decompensation of liver disease
Abdominal mass
Abdominal pain
Weight loss
Bleeding from tumour
36
Q

How is hepatocellular carcinoma diagnosed?

A

Tumour markers: AFP (alpha foetal protein)
Radiological tests: Ultrasound, CT scan, MRI
Liver biopsy done very rarely

37
Q

How is hepatocellular carcinoma treated?

A
  • Hepatic resection
  • Liver transplantation
  • Chemotherapy: Locally delivered TACE (Transcatheter arterial chemo-embolization) or Systemic chemo
  • Locally ablative treatments: Alcohol injection and Radiofrequency ablation
  • Sorafenib (Tyrosinase kinase inhibitor)
  • Hormonal therapy: Tamoxifen

GI Pathology (20 decks)

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