PBL 2- Liver, Bilirubin and Portal Hypertension Flashcards

1
Q

What are the functions of the liver?

A
  • Bile synthesis
  • Glycogen Storage
  • Clotting Factor Production
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2
Q

What are the two liver surfaces?

A

1) Diaphragmatic surface

2) Visceral Surface

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3
Q

Explain the Diaphragmatic surface

A

anterosuperior surface

  • smooth and convex
  • fits between the curvature of the diaphragm
  • ‘bare area’ of the liver- posterior aspect of diaphragmatic surface not in contact with the diaphragm
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4
Q

Explain the Visceral surface

A

posteroinferior surface

  • irregular and flat
  • With exception of fossa of gall bladder and porta hepatis, it is covered with peritoneum
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5
Q

Describe the ligaments of the liver

A

1) Falciform Ligament (curved)- attaches the liver to the diaphragm. Division between the L and R lobes, Contains Ligamentum Teres (remnant of umbilical vein)
2) Coronary Ligament- Attaches superior surface of liver to inferior surface of diaphragm. Separates the bare area of the liver. Anterior and posterior folds unite to form the triangular ligaments on the R and L lobes

Lesser Omentum- attaches liver to the stomach

3) Hepatoduodenal Ligament- Extends from porta hepatis to duodenum
4) Hepatogastric Ligament- Extends from stomach to the liver

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6
Q

Describe the hepatic Recesses

A

anatomical spaces between the liver and surrounding structures

1) Subphrenic spaces- Divided into L and R by the falciform ligament
2) Subhepatic spaces- located between the inferior surface of the liver and the transverse colon
3) Morison’s pouch- potential space between visceral surface of liver and right kidney

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7
Q

Describe the lobes of the liver

A

The lobes are covered by a fibrous layer- Glisson’s capsule. Has a left, right, caudate and quadrate lobe

1) Caudate Lobe- lies between IVC and fossa produced by Ligamentum venosum
2) Quadrate Lobe- lies between gallbladder and fossa produced by ligamentum teres

look at pics

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8
Q

What separates the Caudate and quadrate lobes

A

Porta Hepatis- deep, transverse fissure

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9
Q

What are the liver cells called

A

Hepatocytes

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10
Q

How are hepatocytes arranged, their shape and what are they drained by.

A
Arranged into lobules 
Hexagonal shaped 
Drained by a central vein 
Regenerative ability 
Performs major metabolic functions
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11
Q

Describe a Hepatocyte

A

Hexagonal shaped
1) Has a portal triad at each corner of the hexagon.
Portal TRIAD contains:
- Portal Arteriole: branch of hepatic artery entering the liver
- Portal Venule: Branch of hepatic PORTAL vein entering the liver
- Bile duct: Branch of bile duct leaving the liver

2) Has a singular central vein in the middle of the hepatocyte (looks like a dot)

3) Sinusoids- run from central vein to the portal triads
* look at pics*

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12
Q

What are the acinar zones of the liver and describe them

A

Zone 1- Aerobic reactions, Respiratory chain, Krebs cycle, Fatty acid oxidation, production and bile secretion

Zone 2- ill defined intermediate area

Zone 3- Anaerobic reactions, Glycolysis, Glutamine synthesis and Xenobiotic metabolism

(zone 1 is closest to the portal triads and then zone 2 and zone 3) look at pics

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13
Q

What are Kupffer cells

A

Liver macrophage cells that line the walls of the sinusoids

Function- Phagocytosis

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14
Q

What are Hepatic stellate/ Perisinusodial cells

A

found in the space of Disse. Normally in quiescent phase and store Vitamin A.
However, when Liver is damaged- it is activated and it proliferates. it is responsible for secreting collagen scar tissue which causes cirrhosis.

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15
Q

Describe liver’s blood supply

A

DUAL blood supply

  • Hepatic Artery (25%): supplies O2 to the non-parenchymal cells of the liver (kupffer and hepatic). derived from the coeliac trunk
  • Hepatic Portal Vein (75%): Supplies liver with PARTIALLY deoxygenated blood, delivers to liver parenchyma (hepatocytes). Derived from the stomach, intestine and spleen.
  • -> Hepatic vein drains into the IVC
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16
Q

describe Bilirubin metabolism (STEP 1- RBC breakdown)

A
  • RBCs circulate in the body for 120 days. Macrophages located in the spleen and bone marrow degrade them.
  • RBCs release Hb molecule
  • Hb releases 4x heme and 4x Globin monomers
  • 4x Globin monomers is further broken down into amino acids (re enters blood for erythropoeisis)
  • 4x heme is further broken down into Iron (re enters blood for erythropoeisis) and Porphyrin rings
  • Porphyrin ring broken down to Biliverdin by the enzyme Haem oxygenase
  • Biliverdin broken by Biliverdin reductase enzyme into Unconjugated bilirubin
17
Q

Explain Unconjugated bilirubin solubility

A

HYDROPHOBIC so needs to be carried by the protein albumin to the LIVER for modification and excretion

18
Q

Describe bilirubin metabolism (STEP 2- Unconjugated bilirubin to Conjugated bilirubin)

A
  • Albumin bound Unconjugated bilirubin (UB) transported to hepatocytes by sinusodial bilirubin transporter.
  • UB converted by UDP Glucuronyl Transeferase to Conjugated bilirubin (CB)
  • CB is water soluble
  • CB is excreted by the liver into the bile canaliculi for accumulation in bile within the gall bladder
  • CB in bile travels from the gall bladder to small intestine and then to the Large intestine.
  • CB is converted by intestinal microflora into Urobilinogen. GC acid is a byproduct
19
Q

Describe bilirubin metabolism (STEP 3- Fate of urobilinogen)

A
  • Urobilinogen is lipid soluble
  • 90% of urobilinogen is reabsorbed into the blood stream and into the liver.
  • -> Some of it takes part in the enterohepatic urobilinogen cycle and is re-secreted into bile in the gall bladder.
  • -> The rest travels to the kidneys and is converted into UROBILIN (gives urine its yellow colour)
  • 10% of urobilinogen is oxidised and is converted into STERCOBILINOGEN.
  • stercobilinogen is converted to stercobilin (excreted in faeces, giving its brown colour)
20
Q

Explain the pathophysiology of portal hypertension

A

Cirrhosis is the most common cause of portal hypertension

  • cirhossis causes liver damage/
  • fibrosis and scarring of the liver -> blockage of blood flow through the liver -> portal vein bypass -> increased resistance and pressure in the portal circulation

Due to the backflow of blood and congestion in the portal venous system, blood is forced to find an alternative route back to the systemic circulation, bypassing the liver. This is known as portosystemic shunting (blood away from the liver and towards the heart)

21
Q

What are the complications of portal hypertension?

A

MAIN COMPLICATIONS:

  • Splenomegaly- accumulation of RBCs and WBCs causes spleen to enlarge
  • Hepatic Encephalopathy- confusion
  • Ascites- fluid from blood vessels moves into tissues (VERY bloated stomach)
  • Oesophageal Varices (enlarged veins that are prone to swelling)

OTHER complications:

  • kidney failure
  • Asterixis
  • Gynecomastia (enlargment of breast in males)
  • Spider Angiomata (enlargement of blood vessels close to the skin surface)
  • Palmar erythema (redness of skin in palmar aspect)
  • Hypoalbuminaemia
  • Issues related to coagulation factors
  • Caput Medusae - engorged superficial epigastric veins
  • Hepatomegaly
  • Anorectal varices
22
Q

What are the causes of portal hypertension

A

The causes of Portal Hypertension may be classified as:
(THIS IS NOT SAME AS JAUNDICE)
- Prehepatic (congenital stenosis, portal vein thrombosis, splenic vein thrombosis, extrinsic compression - tumours)
- Hepatic (Cirrhosis, acute alcoholic liver disease, schistosomiasis)
- Post hepatic (Budd-Chiari syndrome – occlusion of hepatic veins, pericarditis)

23
Q

What are the diagnostic techniques used for portal hypertension

A
  • Diagnosed on the presentation of ascites or varices.
  • endoscopy- to check oesophageal varices
  • liver biopsy is the gold standard for cirrhosis so can provide info on the severity of portal hypertension
  • Ultrasound- can show splenomegaly
  • Portal Venous pressure-These can be used to confirm portal hypertension and to differentiate sinusoidal and pre-sinusoidal forms. A balloon catheter is inserted using the transjugular route to measure the wedged hepatic venous pressure (WHVP). Not widely used as it is very invasive
24
Q

Describe the management of portal hypertension

A

Prophylaxis of haemorrhage- Beta Blockers reduce portal venous pressure and the pressure in varices

Acute bleeding:

  • Endoscopic Banding
  • Vasoactive drugs- causes vasoconstriction of varices so prevents bleeding
25
Q

What tests are carried out to check hepatocellular damage?

A

ALT- Alanine Transaminase
AST- Asparate Transaminase
ALP- Alkaline Phosphatase
GGT- Gamma Glutamyltransferase

26
Q

What tests are carried out to check Liver function?

A

Bilirubin
Albumin
Prothrombin Time (PT)

27
Q

What is a useful marker for hepatocellular injury?

A

increased ALT

28
Q

What is a useful marker for cholestasis

A

increased ALP and GGT

29
Q

What can cause increased GGT

A

in response to alcohol, cholestasis or drugs like phenytoin (anti-seizure)

30
Q

WHat causes ONLY an increase in ALP

A

Vit D deficiency, Bone metastases, renal osteodystrophy

31
Q

What causes ONLY an increase in Bilirubin

A

pre hepatic jaundice due to Gilbert’s syndrome or Haemolysis

32
Q

What is indicated if AST > ALT by more than 2:1

A

Cirrhosis or acute alcoholic hepatitis

33
Q

What is indicated if GGT is very raised but ALP is normal/slightly increased

A

Alcohol related