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2nd year > Liver- disease > Flashcards

Liver- disease Flashcards

1
Q

Name the 4 lobes of the liver.

A

Right

Left

Quadrate

Caudate.

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2
Q

What is the function of the gallbladder?

A

Storage of bile

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3
Q

What is the function of the common bile duct?

A

Connects the gallbladder to the pancreas and transports bile to the duodenum.

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4
Q

What is the function of the pancreas?

A

produces digestive enzymes.

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5
Q

What is Jaundice?

A

The accumulation of bilirubin in the circulation

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6
Q

What is bilirubin?

A

A natural product of Haem breakdown which should be in a low level in the blood.

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7
Q

What happens if there is a high level of bilirubin in the blood?

A
  • Bilirubin spreads to the skin and accumulates causing yellow skin.
  • Bilirubin irritates the nerve endings causing itching.
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8
Q

How is bilirubin excreted?

A

It is conjugated by hepatocytes which makes it soluble & able to be excreted.

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9
Q

Discuss the types of jaundice?

A

Pre hepatic- Increased haem load

Hepatic - failure of the liver conjugating the bilirubin

Post hepatic- a blockage of bilrubin removal.

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10
Q

Describe pre-hepatic jaundice

A

Too much bilirubin overloads the livers ability to conjugate it. This results in more unconjugated bilirubin passing in the blood.

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11
Q

Describe how haemolytic anaemia causes pre-hepatic jaundice?

A

There is more red blood cells being broken down quicker than they should be increasing the volume of bilirubin in the blood.

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12
Q

Explain how the mixing of blood at birth causes jaundice? (neonatal cause)

A

The baby’s Blood cells attack and breakdown the mother’s blood cells. Leaving Increased bilirubin in the blood.

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13
Q

What is Kernicterus?

A

Brain damage due to excessive bilirubin deposits in the brain.

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14
Q

Why do we use blue light therapy to treat jaundice babies?

A

The blue light breaks down the bilirubin that has accumulated on the skin surface.

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15
Q

Describe causes of hepatic jaundice?

A
  • Less hepatic cells- so less Bilirubin is conjugated
  • imapaired enzyme action- so less liver cells can conjugate the bilirubin.
  • failure of secretion- Bilirubin is conjugated fine, but the cell membrane is impermeable to conjugated bilirubin .
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16
Q

Describe post hepatic jaundice?

A

This is due to an obstruction in the billary outflow. A blockage in the biliary tree when bile is added results in a backing up of conjugated and unconjugated bilirubin .

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17
Q

What is Primary biliary sclerosis?

A

Autoimmune destruction of the bile duct causing buildup in the liver.

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18
Q

How can a pancreatic carcinoma cause post hepatic jaundice?

A

The tumour squeezes the bile duct and obstructs it

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19
Q

What is a Cholangiocarcinoma?

A

A tumour of the bile duct .

20
Q

What does the dark colour of urine mean?

A

That the bilirubin in the body has been conjuagated.

21
Q

The patient has dark urine and pale stool.

What type of jaundice has caused this? Explain

A

post-hepatic.

The dark urine- bilirubin is conjugated and can make it to the kidney for excretion.

Pale stool- conjugated bilirubin cannot make it to the intestine

22
Q

The patient has dark urine and dark stool.

What type of jaundice has caused this? Explain

A

Pre hepatic jaundice, as the bilirubin has been conjugated, but there is too much bilirubin produced causing the build up.

23
Q

The patient has pale urine and pale stool.

What type of jaundice has caused this? Explain

A

Hepatic jaundice- the bilirubin has not been conjugated, therefore there is no pigment in the urine or stool.

24
Q

How do you treat Post hepatic jaundice?

A
  • Deal with the gallstones:
  • Remove the gallstones by ERCP
  • Remove the gallstones by breaking them up using lithotrispy
  • Force open the channel using a stent (allowing the jaundice to settle before you decide what next)
  • Preventing gallstone reoccurence
25
Q

How do you prevent gallstone production?

A

Removal of the gall bladder (cholecystectomy- no longer able to eat fatty foods)

Prevent bile build up (using medications or altering diet)

Use colestryamine to prevent bile resorption from the GIT.

26
Q

What effect do gallstones have?

A

They block the bilary tree

Cause inflammation of the gallbladder (acute cholecystitis)

27
Q

What are the symptoms of a gallstone?

A

Pain in the shoulder.

Abdominal pain on the right side.

Pain when eating fatty foods.

28
Q

What are acute liver diseases?

A

Acute liver disease is when there is a sudden loss of liver function causing rapid death by:

Bleeding- patient cannot produce more clotting factors once the store has been deplete d

Encephalopathy- damage to the brain due to toxic materials.

29
Q

What is cirrhosis?

A

Mixed damage fibrosis and regeneration of the liver structure which results in an accumulation of damage meaning fewer hepatocytes can eliminate the waste material.

30
Q

What are the signs of cirrhosis?

A
  • Portal hypertension-Blood passing through the oesophagus joining vein producing oesophageal varices which can burst
  • Jaundice
  • Oedema and ascites
  • Encephalopathy- when the liver does not detoxify what you eat
  • palmar ertheyma and spider navi
31
Q

What are these?

and what are they caused by?

A

Spider navi which are enlarged blood vessels.

These are caused by high oestrogen levels.

32
Q

What is this and what causes it?

A

Ascites which is build up of fluid in the abdomen

due to liver failure.

Causing High portal venus pressure.

Low plasma protein synthesis

Low oncotic pressure.

33
Q

What is this and what is it caused by?

A

Palmar erythema

This is caused by enlarged blood vessels due to the high oestrogen levels

34
Q

What are the two functions of the liver and what happens to them when the liver fails?

A

metabolic and synthetic.

These are lost in liver failure.

35
Q

What effect does the loss of synthetic function of the liver have?

A

Liver does not produce clotting factors (concern if taking out teeth)

Does not produce plasma proteins:

  • Transporting proteins
  • Gamma globulin.
36
Q

In liver failure, what processes are affected when we loose metabolic function?

A

Loss of:

Drug metabolism- no first pass mechanism ( so drug dose needs to be altered)

Detoxification

Conjugation of RBC breakdown products (causing jaundice)

37
Q

How do we test liver function?

A

The INR- internal normalised ratio. This measures prothrombin time (time taken to convert prothrombin to thrombin)

It should be 1 (unless patient is on warfarin)

38
Q

What should you ask if you don’t know how bad a patient’s liver problem is?

A

Do they have a specialist doctor for their liver problem?

39
Q

What are the metabolic consequences for the patient of liver disease?

What does this cause?

A

They will have abnormal drug metabolism

This will cause:

  • Prolonged effect of sedative (so avoid IV)
  • Need to reduce drug dosage.
  • Cannot give patient’s tetracycline.
40
Q

What is the most suitable analgesic for a patient with liver disease?

A

Paracetamol .

41
Q

Why do you not give a liver disease patient NSAIDs ?

A

NSAIDs increase bleeding risk.

42
Q

Why are local anaesthetics not a problem for patient’s with liver failure?

A

They are metabolised in the plasma- not the liver.

43
Q

Why does the gallbladder cause pain in the shoulder.

A

Inflammation of the gallbladder causes irritation of the diaphragm and the phrenic nerve. This supplies to skin on the shoulder.

44
Q

What is the main blood supply of the liver?

A

Hepatic portal vein

45
Q

Compare the dental treatment of patients with moderate liver disease to those with severe liver disease?

A

Moderate liver disease :

Platelet count >100

Only one blood cell type is affected.

Can treat patient normally but pack the area after an extraction.

Severe liver disease:

Abnormal blood results.

Difficulty with haemostasis (Stopping bleeding)

Need a haemotologist present to treat (hospital)

2nd year (63 decks)

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