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Spring 4.3 > Liver > Flashcards

Flashcards in Liver Deck (26):

Describe the structure of the liver

Hepatic vein- takes blood back to the heart

Right lobe

Left lobe

Common bile duct

Hepatic artery- brings blood from the heart

Portal vein- brings blood from the bowel


Describe each function of the liver

Metabolism- carbohydrate, fat, protein, steroid hormone, insulin, aldosterone, bilirubin, drugs, vitamin D

Synthesis- plasma proteins (albumin), clotting factors, cholesterol, glucose from fat and protein, urea from amino acids

Immunological- kupffer cells, filter antigens- infection

Secretion- bile and bile salts

Homeostasis- glucose (conversion to glycogen body heat)


What are the top 3 important treatment priorities regarding the liver

Alcoholic liver disease

Metabolic/ NAFLD or NASH

Viral hepatitis- Hepatitis C (HCV)


What is the process for chronic liver damage

Insult e.g. toxin or virus

hepatitis (inflammation) or steatosis (fatty) or steatohepatitis (mixed)

Reversible- liver regeneration

Insult not removed

Fibrosis- thickening and scarring of smooth muscle tissue

Cirrhosis- chronic liver disease


What are the complications of chronic liver damage

Hepatocelluar Carcinoma


What does the term compensated mean in relation to the liver

Known as chronic liver damage but asymptomatic due to medication or enough healthy liver tissue to carry out normal function


What does the term decompensated mean in relation to the liver

When compensated liver disease becomes symptomatic

Ascites- fluid buildup in abdomen

Variceal bleed- When blood pressure increases in the portal vein system, veins in the esophagus, stomach, and rectum enlarge to accommodate blocked blood flow through the liver.

Encephalopathy- changed mental state that can have physical changes

Hepatorenal syndrome (HRS)- consists of rapid deterioration in kidney function


Describe how to grade cirrhosis levels

Child's pugh
A= 5-6 points (compensated)
B = 7-9 points (moderate)
C= 10-15 points (advanced)

- does not predict drug handling

Prothrombin Time/INR


Describe acute liver failure grading in terms of HYPERACUTE.

Time from jaundice to encephalopathy- 6 to 7 days

Cerebral oedema- common

Renal failure- early

Ascites- rare

Coagulation disorder- marked

Prognosis- moderate


Describe acute liver failure grading in terms of ACUTE

Time from jaundice to encephalopathy- 8 to 28 days

Cerebral oedema- common

Renal failure- late

Ascites- rare

Coagulation disorder- marked

Prognosis- poor


Describe acute liver failure grading in terms of SUBACUTE

Time from jaundice to encephalopathy- 29 to 84 days

Cerebral oedema- rare

Renal failure- late

Ascites- common

Coagulation disorder- modest

Prognosis- poor


What are causes of liver disease. Chronic (7) Acute (6)

1. Alcohol

2. Non alcoholic fatty liver disease (NAFLD)/ Non alcoholic steatohepatitis (NASH)

3. Metabolic e.g. haemochromatosis, wilsons, alpha-1 antitrypsin deficiency

4. Drugs

5. HCV, HBV (hepatitis B and C)

6. Malignancy

7. Unkown

1. Hepatitis HAV, HBV, HEV (3rd trimester of pregnancy)

2. Drugs like paracetamol, ecstasy

3. Infection e.g. CMV malaria

4. Ischaemia

5. Alcoholic hepatitis

6. Acute fatty liver of pregnancy


What are alcohol related complications (4)

1. Acute alcohol withdrawal, seizures, Delirium Tremens (confusion)

2. Wernike's encephalopathy- presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B1).

3. Liver disease

4. Acute and chronic pancreatitis


Describe what is non-alcoholic fatty liver disease (NAFLD) (4)

1. Spectrum of liver diseases ranging from simple fatty liver through to non alcoholic seato-hepatitis (NASH) to fibrosis and cirrhosis

2. More common if you are type 2 diabetic, metabolic syndrome

3. Rate of progression variable

4. Associated with excessive liver and cardiovascular morbidity/mortality + excess mortality from cancer


How do you assess and manage non-alcoholic fatty liver disease (NAFLD) (8)

1. Weight loss- lifestyle, fish and veg

2. 2-3 cups of coffee a day

3. Exercise- reduce fatty liver content

4. Lack of evidence with omega 3-FA

5. Reduce and stop alcohol and smoking

6. Statins- only stop if liver function tests double within 3 months of starting

7. Pioglitazone/vitamin E- if advanced fibrosis

8. Cardiovascular- antihypertensive


Describe how hepatitis C works, transmission (5), diagnosis and what to do if positive

RNA virus that spreads by infective hepatic cells then rapidly replicating- blood bourne virus

Can lead to development of cirrhosis

Transmission through:
Sharing same toothbrush
Blood transfusion

Dry blood spot test or saliva- antibodies
Serum blood- antibodies or antigens

If positive:
blood viral RNA (virus present) and genotype
Fibroscan (nb other cofactors)
Refer for treatment with oral directly acting anti-virals (8 to 16 weeks)


Describe how hepatitis B (HBV) is transmitted and what it can progress to

Transmitted by blood and bodily fluids- childbirth, casual sex, close family members

5-10% infected can't clear it and become carriers (in blood for 6 months or more) leading to chronic infection

Can progress to liver fibrosis or cirrhosis or Hepatocellular carcinoma (HCC)


Describe the use of liver function tests (6)

Identifies patients suffering from liver or biliary tract disease

Not specific

Some LFTs reflect liver damage rather than function

In normal range despite underlying disease or abnormal in asymptomatic patients

Look for trends

Concern if 3 times the upper normal limit


What are the liver damages that liver function tests can identify (3)

Acute Hepatoceullar Damage (paracetamol)
- Rise in plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST)
- Secondary rise in Bilirubin (unconjugated)
- Prolonged PT
- Normal albumin (long half life)

Chronic hepatocellular damage (cirrhosis)
- Normal(ish) ALT and AST
- Low albumin and prolonged prothrombin

Chloestatsis (blockage of bile duct)
- Rise in plasma Alkaline phosphatase (ALP) and bilirubin (conjugated)


What are the abnormal liver function tests that are investigated and what changes could indicate which liver disease

Clinical- alcohol or drugs

Other bloods- FBC, clotting, U and Es

USS liver (imaging technique) to exclude Common bile duct (CBD) dilatation and portal hypertension, hepatocellular carcinoma (HCC)
MRCP/CT scan then Endoscopic retrograde cholangiopancreatography (ERCP)

Liver screen if ruled out obstruction
- Virus- hepatitis B or C if viral DNA present
- Autoantibodies- positive in autoimmune primary biliary cholangitis (PBC), chronic hepatitis diseases
- Immunoglobulins
- Serum ferritin
- Alpha antitripsen- deficiency= liver disease in infancy and cirrhosis in adults
- Alpha fetaprotein- hepatoma


What are common diagnostic tests used (5)

- Cause vs assess damage
- Bile duct leak, bleeding

- Measures liver stiffness
-non invasive

- identify extra-hepatic duct dilatation
- Other abnormalities- cysts, tumour

Magnetic resonance cholangiopancreatography (MRCP) /endoscopic retrograde cholangiopancreatography (ERCP)
- Pancreatic/billary disease (investigates billary obstruction)

Viral PCR
- HCV or HBV


How does drug indued liver injury occur and what does it increase in and what mechanisms does it involve

Caused by drugs including herbal remedies

Increases risk with age, female, genetics, alcohol, previous exposure, pre-existing liver disease, concomitant drugs, renal failure/diabetes, enzyme induction, pregnancy, poor nutrition, poly pharmacy

Several mechanisms- cytochrome p450, immune mediated damage to cells

Mimic almost every natural occurring liver disease- clinical features vary depending on damage

Leads to medications removed from market or black box warnings



Describe the two type of hepatotoxins

Intrinsics (TYPE A):
Predictable, dose dependent, reproducible
Short incubation period (hours or weeks)
Drug examples: paracetamol, tetracycline, salicylates, MTX, alcohol, iron, vitamin A, cyclophos, anabolics
Can occur at lower doses if you have pre-existing liver disease
Necrosis= type of injury
Direct toxicity

Idiosyncratic (type B)
Unpredictable, not dose related, injury variable, rare, more frequent in pre-existing liver disease
- Incubation typically weeks or months
- Any type of liver injury
- Due to hypersensitivity like methyldopa or metabolic abnormality (isoniazid)


Explain what direct insult leads to (steps)

Direct insult leads to drug induced hepatotoxicity, leads to
Cytotoxic cellular destruction
Cholestatic- impaired bile flow

All lead to:
Necrosis and/or steatosis (cell death or fatty degeneration)


Explain how acetaminophen (paracetamol) leads to a non toxic and toxic compound

Acetaminophen can conjugate into:
glucuronide- moiety (non toxic)
sulfate- moiety (non toxic)
N-acetyl-p-benzo-qunone mine NAPQI (toxic)

This NAPQI can be converted to cysteine and mercapturic acid conjugates that are non toxic via glutathione with NAC


What could the pharmacist do if you think a drug could be the cause of induced liver injury

Review all potential medicines taken- herbal, OTC, P, POM, vitamins

Still taking which drugs
- Frequency, dose

Started, stopped
Drug reactions occur within first 3-6 months treatment (5-90 days from first dose, 15 days from last dose)

Presenting signs and symptoms
- pattern of liver disease- pre-treatment
- suspect drug if presents with jaundice until proven otherwise
- some can cause jaundice, others none