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Met2 > Liver and liver disease > Flashcards

Liver and liver disease Flashcards

1
Q

What are the functions of the liver?

A
  • protein metabolism
  • hormone and drug inactivation
  • immunological function
  • formation of bile
  • lipid metabolism
  • carbohydrate metabolism
  • form coagulation factors
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2
Q

What are the different liver function tests?

A

albumin (protein synthesis)

coagulation (PT, INR)

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3
Q

What are the different liver biochemistry tests?

A
  • AST (if AST>ALT = alcohol-induced hepatitis)
  • ALT (if ALT>AST = viruses/non-alcoholic fatty liver disease)
  • alkaline phosphatase (elevated = biliary obstruction)
  • gamma glutamyltransferase(elevated = chronic viral hepatits)
  • bilirubin (elevated = jaundice)
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4
Q

How are units of alcohol calculated?

A

units = strength (ABV) x volume (ml)/1000

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5
Q

Describe the metabolism of alcohol.

A

ethanol –alcohol dehydrogenase–> acetaldehyde –aldehyde dehydrogenase–> acetate

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6
Q

What is the result of:

  • increased acetaldehyde
  • increased acetate
  • increased NADH
A
  • increased acetaldehyde: uncoupling of mitochondria = reduced ATP
  • increased acetate: more fatty acid production
  • increased NADH: more G3P production
    END RESULT: more triglycerides and reversible cell injury
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7
Q

What are the consequences of alcohol-induced liver damage?

A
  1. alcoholic fatty liver
    - asymptomatic fat deposits in liver
    - liver enzymes normal/moderately raised
    - liver will be slightly enlarged and pale yellow
    - microanatomy: fat deposits in hepatocytes, especially zone 3
  2. alcoholic hepatitis
    - painful hepatomegaly
    - fever
    - lots of mallory bodies, neutrophils, hepatocyte swelling
    - raised AST, raised ALT therefore raised AST:ALT
    - raised gamma GT (alcohol causing microsomal hyperplasia)
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8
Q

How is alcoholic hepatitis managed?

A
  • lifelong alcohol abstinence is vital
  • steroids may help in severe cases
  • supplements if liver function is permanently compromised
  • encephalopathy (deficiency in ammonia removal)
  • coagulopathy (deficiency in clotting factors)
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9
Q

What is hepatic encephalopathy? How is it diagnosed and treated?

A
  • precipitated by sepsis, bleeding, drugs (opioids, benzodiazepines), deteriorating liver function
  • presents as mild confusion –> coma

Diagnosis:

  • hepatic flap
  • clinical symptoms
  • EEG/MRI changes

Treatment:

  • lactulose
  • transplantation
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10
Q

What is haematemesis a sign of? How is it managed?

A

Sign of a complication of fibrosis:

  • portal HTN
  • variceal bleeding from lower oesophagus

Management:

  • resuscitation (blood or albumin)
  • correct clotting factor abnormalities
  • IV terlipressin: splanchnic vasoconstrictor
  • endoscopic banding or scleropathy
  • emergency portosystemic compression (sengstaken-blakemore tube)
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11
Q

Describe the different portosystemic shunts.

A
  1. oesophageal branch of left gastric vein anastomoses with oesophageal branch of azygos vein –> can pop if engorged with blood
  2. Paraumbilical vein of HPV anastomoses with superficial epigastric branch of femoral vein
  3. superior rectal vein of IMV anastomoses with inferior and middle rectal veins of internal pudendal vein
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12
Q

What is the most common chronic blood infection?

A

Hepatitis C

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13
Q

What causes hepatitis C?

A

drug use
unprotected sex
transfusion

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14
Q

What family of viruses dos hepatitis belong to?

A

Flavivirus family

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15
Q

What is the incubation period of HCV?

A

~2 months

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16
Q

Compare the acute and chronic presentation of HCV.

A

Acute:

  • asymptomatic (85%)
  • reduced appetite, reduced weight, muscle ache, nausea and fatigue
  • raised AST > increased ALT
  • inflammatory infiltrate (mainly CD8+ cells removing hepatocyte intracellular infection)
  • councilmann bodies (apoptosis eosinophil-like hepatocytes)

Chronic:

  • > 6 months
  • Fatigue + mild cognitive dysfunction
  • S+S:
    1. palmar erythema
    2. spider naevi
    3. hair loss
  • -> if all 3 S+S = 80% chance of liver disease
    4. leuchonychia
    5. proximal easting
    6. stretch marks
    7. xanthelasma (yellowish deposit of cholesterol underneath skin)
  • portal triad inflammation
17
Q

What is pruritis?

A

itching (bile irritates the skin)

18
Q

What are S+S of damage to the gallbladder/cholestatic symptoms?

A
  1. pruritis

2. pale stools + dark urine

19
Q

How is HCV diagnosed and managed?

A

Diagnosis:

  • HCV IgG antibody enzyme immunoassay (ELISA) –> can’t differentiate acute, chronic or resolved
  • PCR to detect HCV RNA (GOLD STANDARD)
  • Liver biopsy - can assess degree of liver damage

Treatment:

  • depends on serotype
  • 95% cure rate (e.g. Sofosbuvir/velpatasvir)
  • treatment for ~12 weeks
20
Q

What can cause hepatocellular carcinoma?

A
  • cirrhosis

- hep B+C

21
Q

What are the causes of cirrhosis?

A
  • haemachromatosis
  • Wilson disease (increased copper in blood)
  • alpha-1 antitrypsin deficiency
  • fat
  • viral hepatitis
  • biliary disease
  • autoimmune disease
  • alcoholic/non-alcoholic fatty liver disease
22
Q

What are the clinical and biochemical findings in hepatocellular carcinoma?

A
  1. nodules on free edge of liver (palpation)
  2. portal hypertension: backlog of blood, ascites, tender hepatomegaly, splenomegaly, hepatorenal syndrome
  3. reduced detoxification:
    - jaundiced (bilirubin)
    - mental status changes (ammonia)
    - gynaecomastia, spider naevi (oestrogen)
  4. reduced protein synthesis
    - hypoalbuminaemia (exacerbate ascites)
    - coagulopathy
  5. Albumin <28g/L
  6. Prolonged PT
  7. liver biochemistry = compensated normal
    - Decompensated: raised AST, ALT, ALP and gamma GT
23
Q

What investigations are carried out for hepatocellular carcinoma?

A
  1. raised alpha-fetoprotein
  2. US or contrast CT/MRI
    - -> contrast MRI = GOLD STANDARD
  3. biopsy –> only when you can’t diagnose via MRI, want to avoid –> can help spread the cancer
24
Q

How is HCC managed?

A
  1. surgery (lobe resection)/liver transplant
  2. percutaneous ablation (ethanol injection/US probes)
  3. transarterial chemoembolisation (if someone can’t have ablation)
    - injection of chemotherapeutic agents (hepatic artery) and embolising agents (blocks blood supply to tumour)
25
Q

What is the prognosis for HCC?

A

~6-20 months

–> often detected late as symptoms are masked by cirrhosis

26
Q

How can HCC be prevented?

A
  • vaccination
  • screening cirrhosis patients (every 6 months)
  • alcohol abstinence
27
Q

When are liver transplants indicated?

A
  • metabolic conditions
  • autoimmune
  • alcoholic liver disease
  • biliary (Primary sclerosing cholangitis, Primary biliary cholangitis)
  • Hep C
  • Cancer
  • Paracetamol poisoning (give NAC)
28
Q

What are the different types of transplant?

A
  • orthostatic transplant (cut diseased bit straight out)
  • living donor transplant
  • split transplant (usually for children - use left side)
29
Q

What drugs are used as immunosuppression after a liver transplant?

A
  • calcineurin inhibitors
  • sirolimus
  • anti-proliferative purine inhibitors
  • steroids
30
Q

What are the S+S of compensated liver disease?

A
  • xanthelasma
  • parotid enlargement
  • spider naevi
  • gynaecomastia
  • splenomegaly
  • palmar erythema
  • clubbing
  • dupuytren’s contracture
  • xanthomas
31
Q

What are the causes of decompensated liver disease?

A
  • sepsis (ascitic tap)
  • bleeding
  • HCC
  • venous occlusion
  • drugs (NSAIDs)
32
Q

What are the symptoms are associated with decompensated liver disease?

A

Neurological:

  • disorientation
  • drowsy –> coma
  • hepatic flap
  • fetor hepaticus

General:

  • ascites
  • oedema
  • dilated veins on abdomen
33
Q

What are the general signs of decompensated liver disease?

A
  • jaundice
  • fever
  • loss of body hair
34
Q

What is used to treat encephalopathy?

A

lactulose (reduce colon absorption of ammonia and helps clear bowels)

35
Q

What is the diuretic of choice for portal hypertension?

A

spironolactone

36
Q

What is the pathophysiology of ascites and hepatorenal syndrome?

A
  • portal hypertension
  • splanchnic vasodilation
  • reduced effective circulatory volume
  • activation of RAAS
  • renal Na+ avidity = ASCITES
  • renal vasoconstriction = HEPATORENAL SYNDROME
37
Q

What is the treatment for ascites and hepatorenal syndrome?

A
  • low salt diet

- diuretics (spironolactone)

Met2 (26 decks)

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