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AI Exam 2 > Liver > Flashcards

Liver Flashcards

1
Q

What are the three types of metabolism that the liver is involved in?

A

Carbohydrate
Lipid
Protein

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2
Q

How does the liver contribute to immunity?

A

Reticuloendothelial system
Kupffer cells
Hepatic stellate cells.

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3
Q

What substances does the liver store?

A

Fats,
Glycogen,
Trace elements like copper and iron,
Vitamins A, D, K and some B vitamins

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4
Q

What role does the liver play in detoxification?

A

Converts ammonia to urea
Detoxifies drugs and xenobiotics through Phase 1 and Phase 2 reactions

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5
Q

What does the liver synthesise?

A

Hormones, Plasma proteins and bile acids

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6
Q

What is the endocrine function of the liver?

A

Modifies Vitamin D3 and Thyroid hormone T4 to T3
Degradation of hormones

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7
Q

What is the function of bile and where is it stored?

A

Stored in the gallbladder
Helps in digestion and absorption of fats

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8
Q

What are bile salts and what is their function?

A

Bile salts help convert large fat globules into a liquid emulsion called a micelle.

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9
Q

How is bilirubin excreted?

A

Bilirubin is converted to urobilinogen and then to stercobilin which is excreted into faeces.

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10
Q

How are RBCs and Hemes broken down in the liver?

A

1) RBCs are broken down into Heme,
2) Broken down to bilirubin
3) Bilirubin is converted to urobilinogen and stercobilin.

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11
Q

What characterises acute liver disease?

A

Self limiting
Hepatocyte inflammation and damage,
Can cause liver failure
Aetiology - drugs or viruses

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12
Q

What are the symptoms of acute liver disease?

A

Asymptomatic or:
generalised malaise, anorexia, fever and later-stage jaundice

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13
Q

How is chronic liver disease defined?

A

Lasts over 6 months,
Leads to permanent damage and cirrhosis
Cause: Alcohol abuse

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14
Q

What symptoms are associated with chronic liver disease?

A

Fatigue, weakness, weight loss, nausea, vomiting, loss of appetite, cachexia, abdominal swelling, right upper quadrant pain, jaundice and bleeding disorders.

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15
Q

What is the progression of liver damage?

A

1) Chronic injury
2) Early fibrosis and disrupted liver architecture,
= irreversible liver failure and portal hypertension.

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16
Q

What is fatty liver and how does it differ from advanced fibrosis?

A

Fatty liver is reversible condition with triglyceride fat accumulation in liver cells. Advanced fibrosis is a late stage of liver damage characterised by significant structural changes and cell death.

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17
Q

How does alcohol consumption cause liver damage?

A

Alcohol causes inflammation that can progress to fatty liver and fibrosis

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18
Q

What causes jaundice in liver disease?

A

A build up of bilirubin due to haemolysis, hepatocellular damage or cholestasis.

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19
Q

What leads to the development of ascites?

A

Ascites is caused by portal hypertension, low plasma albumin and salt and water retention by the kidneys.

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20
Q

What are oesophageal varices and how do they form?

A

Oesophageal varices are swollen veins in the oesophagus caused by increased pressure in the portal vein

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21
Q

What is hepatic encephalopathy and what worsens it?

A

Build-up of ammonia in the blood, it can be worsened by dehydration, GI bleeds and increased dietary protein.

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22
Q

What blood test results indicate if the liver is working?

A

Albumin and Clotting (PT)

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23
Q

What blood test results indicate liver damage?

A

ALT, AST, GGT, ALT/AST ratio

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24
Q

What blood test results indicate liver secretion?

A

Bilirubin, ALP and GGT

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25
Q

What factors can alter drug clearance, biotransformation and pharmacokinetics in liver disease?

A

Intestinal absorption,
Plasma protein binding,
Hepatic extraction ratio,
Liver blood flow,
Portal-systemic shunting,
Biliary excretion,
Enterohepatic circulation,
Renal clearance.

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26
Q

What are the Phase 1 metabolic processes in the liver and examples of drugs for each?

A

Oxidation (Azathioprine),
Reduction (Halothane),
Hydrolysis (Atropine, Pethidine).

27
Q

What are the Phase 2 metabolic processes in the liver and examples of drugs for each?

A

Glucuronidation (Paracetamol, Morphine),
Sulphonation (Steroids),
Acetylation (Hydralazine, Phenelzine),
Methylation (Nicotine).

28
Q

How does a high extraction ratio differ from a low extraction ratio in liver disease?

A

High extraction ratio means clearance depends on hepatic blood flow,
Low extraction ratio means clearance depends on the metabolizing capacity of the liver.

29
Q

How should drugs be adapted for a patient with liver impairment?

A

Side effects the patient experiences

30
Q

What effect does a CYP450 inhibitor have on drug levels?

A

increase

31
Q

How does liver disease affect pharmacodynamics?

A

Increases sensitivity to drugs that affect clotting/bleeding, CNS, and diuretics due to decreased production of clotting factors, hypovolemia, and hypokalemia.

32
Q

What is the significance of GGT levels in patients on CYP450 inducers?

A

An increase in GGT levels can indicate that a patient is on a CYP450 inducer.

33
Q

What is the impact of liver disease on constipation?

A

Nitrogenous waste products remaining in the gut for longer periods.

34
Q

What are the minor symptoms of acute alcohol withdrawal?

A

CNS hyperactivity resulting in indomnia, temulousness, mild anxiety, GI upset, headache, diaphoresis, palipitations,

35
Q

Chronic alcoholics when in withdrawal can have seizures, true or false?

A

True

36
Q

What is given to patients in acute alcohol withdrawal?

A

Benzodiazepines such as Chlordiazepoxide, Oxazepam on a reducing regiment over 9 days.

37
Q

What is the treatment for Cholestatic Pruiritis?

A

1st Cholestyramine
+ Antihistamines
+Topical treatment for irritation

38
Q

What causes Ascites?

A

High aldosterone (RAS), causes fluid retention, as the liver would metabolise but liver function is reduced causing an accumulation of aldosterone.
+ Reduced albumin, which reduces osmotic pressure causing oedema and fluid.

39
Q

What is the treatment for Ascites?

A

1st line - Spironolactone
+Furosemide if no weight loss/peripheral oedema or swap to if optimised spironolactone is not working.

40
Q

What is the aim for Weight-loss with a patient with Ascites?

A

0.5-0.75kg reduction per day, if the patient has peripheral oedema 1-1.5kg per day.

41
Q

What is the treatment for Wernicke-Korsakoff Syndrome?

A

IV Pabrinex and Thiamine 100mg TDS for 3-6 months.

42
Q

What causes hepatic encephalopathy?

A

Ammonia bypasses the liver and blood can’t get through, ammonia then passes the BBB.

43
Q

What are the steps of Hepatic Encephalopathy?

A

1- Disaccharide breaks down, pH in intestine to 5, ionisation can occur and less absorption.
2- Intestinal flora altered, reduces ammonia producing bacteria in the gut
3 - Speeds gut transit time, less time for nitrogenous ammonia waste to be in the gut and then absorbed.

44
Q

What is the treatment for Hepatic Encephalopathy?

A

1st - Lactulose 30-50ml TDS
AIM: 2-3 soft stools daily
ADD Rifaximin if lactulose isn’t working.
2nd - Phosphate Enema’s if can’t tolerate lactulose

45
Q

What is portal hypertension?

A

Elevated pressure in the portal vein, the blood vessel that carries blood from the bowel and spleen to the liver. This is commonly caused by cirrhosis and can cause internal bleeding.

46
Q

How do you treat portal hypertension?

A

First line: Low dose propranolol and increase this cautiously
Second line: Other vasodilators *Nitrates

47
Q

How do you treat Bleeding Oesophageal Varices?

A

1st line - Vasoactive therapy (Vasopressin, terilpressin and octreotide)

48
Q

If a patients PT is more than 18 seconds what treatment should be given, and what should be avoided?

A

Give IV Phytomenadione
AVOID - Aspirin, NSAIDs and Warfarin

49
Q

What are the pathophysiologic mechanism’s to Hepatotoxicity?

A

-Disruption of the hepatocyte
-Disruption of the transport proteins
-Cytolytic T-Cell activation
-Apoptosis of hepatocytes
-Mitochondrial disruption
-Bile duct injury

50
Q

What are the features of ADR Type A?

A

-Intrinsic or predictable
-Reproducible injury in animals
-Due to drug or metabolite
-80% of all ADR
-Paracetamol or carbon tetrachloride

51
Q

What are the features of ADR Type B?

A

-Idiosyncratic or unpredictable
-Hypersensitivity or immunoallergenic eg, phenytoin with fever, rash, eosinophilia.

52
Q

What can happen to LFT’s during Hepatotoxicity?

A

Can increase up to 2x the reference range!

53
Q

What is the management of Hepatotoxicity?

A

-Drug removal
-Antidote if appropriate
-Corticosteroids
-Supportive therapy
-Yellow card scheme

54
Q

How many grams of paracetamol can cause fatal hepatic necrosis?

A

15

55
Q

how many grams of paracetamol can cause a risk of severe liver failure?

A

7.5

56
Q

how many grams of paracetamol requires hospital admission and observation?

A

5

57
Q

What do you measure to test for paracetamol overdose?

A

Serum Paracetamol Concentration

58
Q

What is phase 1 of hepatotoxicity?

A

0.5-24 hours after ingestion, asymptomatic or nausea, vomiting, malaise

59
Q

What is phase 2 of hepatotoxicity?

A

18-72 hours after: RUQ Abdo pain and tenderness, anorexia, nausea, vomiting, lack of urine output

60
Q

What is phase 3 of hepatotoxicity?

A

Hepatic phase, 72-96 hours after ingestion: continued symptoms, hepatic necrosis may be seen as jaundice, coagulopathy, hypo’s, hepatic encephalopathy, possible acute renal failure, and death from multi-organ failure.

61
Q

What is phase 4 of hepatotoxicity?

A

Recovery, 4 day to 3 week after, complete resolution if survive phase 3.

62
Q

Why is paracetamol overdose so dangerous to the liver?

A

-Paracetamol normally conjugates with gluconide which is then excreted in the urine, -BUT 5% is metabolised to NAPQI which is toxic, at normal levels this is ok as it is detoxified by conjugated with glutathione and then being excreted via urine.
-In overdose levels, glutathione stores are depleted fast and now it binds directly to the hepatocytes and causes cell damage.

63
Q

How do we treat paracetamol overdose?

A

1st line - IV Acetylcysteine and Oral Methionine to replenish Glutathione Stores!
*12 hours post ingestion antidote is less effective.
Dosing is dependent on plasma concentration and hours after ingestion

64
Q

What effect does a CYP450 inducer have?

A

Reduces drug levels

AI Exam 2 (16 decks)

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