Liver diseases Flashcards

1
Q

What are the different types of liver disease?

A

1.Alcoholic Liver Disease- 2.5 million deaths
2.NAFLD-1 in10
3.Viral hepatitis- B=290 million c= 200 million 900k deaths due to B
4.Drug-induced toxicity- Paracetamol overdose
5.Hepatic Carcinoma- 5th common cancer

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1
Q

What are the causes of Pre-hepatic, Hepatic and Post-Hepatic?

A

1.Pre-hepatic-Haemolytic, Newborn &Genetic
2.Hepatic-Alcohol, viruses , diets & drugs
3.Post-Hepatic- Gallstones & tumours

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2
Q

What happens in alcohol liver disease (ALD) and what is the treatment?

A

1.Alcohol is sent to the liver for processing
Excess can cause liver disease

2.Alcohol enters the liver cells or hepatocytes it takes on of the three pathways
a. Use of ADH
b. CATALYSE- PERSXISOME
c. Cytochrome p450 2e1
These all lead to the conversion of alcohol to acetaldehyde

3.When ADH coverts the alcohol to acetaldehyde it needs another compound NAD which is converted to NADH. NADH levels increase and the NAD levels decrease it has an effect

4.The increase in NADH tells cells make fatty acid and the decrease in NAD tells cells produce less fatty acid oxidation leading to more fat production in the liver = fatty liver so it becomes large in size , making it heavy greasy and tender the liver becomes yellow and there are other symptoms that are not present

Treatment- decrease alcohol intake

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3
Q

What are the happens of acute Alcohol Poisoning/intoxication and what can cause it ?

A
  1. Coma
    2.Low respiration
    3.Vomiting- choke
    4.Low body temp, Cold
    5.Low BP/low heart rate

Binge drinking can lead to acute alcohol poisoning

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4
Q

How does chronic ALD happen?

A

Through excess alcohol intake over the years

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5
Q

What parts of the body does liver damage effect ?

A

1.Heart(Dilated cardiomyopathy
2.Pancreas(acute/chronic
3.Brain(damage, poor memory)
4.Skeletal muscle – type I & II fibres
5.Bone(osteoporosis
6.Foetus

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6
Q

What are the cofactors of ALD?

A

1Nutrition(dietary fat/iron)
2. Genotype for alcohol dehydrogenase, CYP2E1
3. Viral hepatitis
4. Gender
These co-factors increase the risk of ALD

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7
Q

What are the ALD stages?

A

1.More drinking leads to AH then Fibrosis and cirrhosis which is where the liver is failing
Cirrhosis- caused my alcohol abuse
Ah- is inflammation to the liver

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8
Q

What happens in alcoholic hepatitis and what is the treatment?

A

1.Acetaldehyde from ethanol it starts to generate reactive oxygen species which are reactive and have o2 e,g hydrogen peroxide

2.These reactive oygen species react with proteins and dna causong damage to the cells

  1. Acetaldehyde can bind to macromolecules and cell membrane inhibiting the molecule forming Acetaldehyde adduct

4.The immune system recognises the new compounds as foreign so the neutrophils to clean it up it destroys the hepatocytes and the liver inflammated and damaged which is AH

Treatment;
Stop alcohol and supress immune system tablets
More damage leads to cirrhosis and liver failure

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9
Q

What is NADH role in the electron chain?

A

Nadh fuels electron flows in the electron transport chain in the mitochondria- electrons are leaking out of the chain

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10
Q

How does the liver get nutrients?

A

Nutrients from gut goes through the portal vein and transports it to the liver

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11
Q

What are the two stage in alcohol cirrhosis and what do they do?

A
  1. Compensated- the liver is still function 70% loss of the function but can still work

2.Decompensated- not stability patient needs liver transplant - loss of function

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12
Q

What is NAFLD/MAFLD and what are the stages?

A

NAFLD/MAFLD is a liver disease caused by diet
Health -> non-alcoholic fatty liver (Benign tumour but no liver damage) –> non-alcoholic steatohepatitis (Liver inflammation leading to fibrosis) –> cirrhosis

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13
Q

What causes NASH non-alcoholic steatohepatitis, what it lead to and how is it diagnosed?

A

Caused by excess dietary energy intake
Leads to lobular necroinflammatory hepatitis decreasing the function

it is diagnosed be Liver biopsy there are non biochemical markers

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14
Q

Who has the highest level of billirubin and how can it be broken down?

A

New borns- if it is way to high it can lead to brain damage
It is broken down by UV light/ blue light

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15
Q

What are the factors affecting bilirubin measurement?

A

*Light
* Biological variation
* Haemolysis- Hb interference
* Fasting
* Race- lower in African-Americans

16
Q

Where is bilirubin and what effect does it have?

A

1.In healthy individuals conjugated Bilirubin is undetected in the urine (and serum)

Bilirubinuria increase in the plasma concentration of conjugated

17
Q

What are the observations of conjugated hyperbilirubinaemia?

A

1.Hepatocyte damage – leakage from hepatocyte & Increased urine detection of conjugated water soluble bilirubin (orange/brown colour)

2.Biliary system blocked - no bilirubin in gut - faeces pale colour

18
Q

What are the alcohol markers

A

Blood (24-36h)
Breath (1-12h)
Urine (24-48h)
Saliva (24-26)

19
Q

What is the information of transferrin?

A

1.Is a glycoprotein
2. Single polypeptide chain of 679 a/acids
3.Two iron binding sites,
4. Eliminated by the liver via lysosomal degradation
5.Oligosaccharide units have stabilising functions andmay affect receptor affinity

20
Q

How is fibrosis diagnosed?

A

Via fibrosa - which measures the rigidity/stiffness of the liver

21
Q

What is the key information about ammonia?

A

1.Produced in the gut, and absorbed into portal venous system, transported to the liver ,and detoxified into urea and aa’s

  1. Ammonia levels rise in liver diseases e.g Hepatic failure
22
Q

What are the acute hepatitis symptoms ?

A

1.Fever
2.Jaundice
3.Flu like symptoms in the nose
4. Weakness
5.Weight loss
6.Diarrhea
7. Dark or brown urine

23
Q

What are the key facts of Hepatocellular Carcinoma (HCC)

A
  • Long Asymptomatic stage lasting 2 years or more
  • Early detection possible in patients with chronic HBV/HCV
  • Ultrasound less sensitive and specific in detecting HCC in cirrhotic livers, due to increased echo-density from regenerating nodules ,giving false positive results
  • Activation of host growth factors (oncogenes)
  • Necroinflammation activates host growth factors
23
Q

Factors affecting ALP?

A

*BMI
* Food consumption
* Haemolysis- Hb inhibits
* Race- higher in African-American men
* Pregnancy - increase
* Bone disease -increase
* Stability-fridge/freezer