Alcohol Related Liver Disease Flashcards

Caoimhe

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1
Q

Functions of Liver (4)

A
  1. Metabolism: (of lipids, proteins, hormones, CHOs, drugs, toxins, foreign compounds)
  2. Synthesis: (of cholesterol, clotting factors, plasma proteins)
  3. Storage: (of glycogen, vitamins, minerals)
  4. Metabolism and excretion of bilirubin
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2
Q

4 Stages of ARLD

A
  1. Steatosis: fatty build up in liver
  2. Acute and chronic alcoholic hepatitis
  3. Fibrosis: any degree of scarring in liver
  4. Cirrhosis: due to long term damage, extreme scarring, will result in liver failure, irreversible
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3
Q

Why is the liver the major organ target of alcohol induced injury?

A

Because the liver is the main site of alcohol metabolism

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4
Q

What is steatosis?

A

Fatty build up in the liver, usually resolves upon cessation of alcohol consumption

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5
Q

What is fibrosis?

A

Fibrosis describes any degree of scarring in the liver. It can be reversed if aetiological agent is removed.

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6
Q

what is cirrhosis?

A

More extensive scarring accompanied with regenerative nodules

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7
Q

Pathogenesis of steatosis

A
  • The hepatitis fatty acid (FA) pool is a balance of FA influx from diet, adipose tissue lipolysis, creation of new lipids and disposal of FAs.
  • An increased uptake and reduced clearance of FAs leads to accumulation of lipids and development of steatosis.
  • Alcohol interferes with lipid metabolism: the breakdown of alcohol by ADH releases NADH causing the cell to inhibit the breakdown of FAs while simultaneously to increase the synthesis of FAs, creating more lipids than needed and leading to a false sense of energy.
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8
Q

ARLD pathogenesis

A
  • ADH pathways overwhelmed so alcohol oxidation by MEOS and catalase increases
  • The MEOS and catalase pathways are more likely to produce harmful by-products that contribute to inflammation
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9
Q

ARLD pathogenesis expanded (3)

A
  1. Alcohol mediated liver steatosis
  2. Inflammatory immune response and oxidative damage
    3.Intestinal permeability and consequent intestinal microbiome changes
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10
Q

Intestinal permeability changes lead to an increased risk of ??

A

Infection (due to bacterial overgrowth) and pro inflammatory changes

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11
Q

ARLD risk factors (5)

A
  1. **Increased alcohol consumption
  2. obesity
  3. genetics**
  4. being african/hispanic
  5. being female
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12
Q

Signs and symptoms (7)

A
  1. Abdo pain and tenderness: inflammation of liver due to steatosis
  2. Dry mouth
  3. Anaemia: due to liver having an input in iron homeostasis
  4. Skin colour changes (jaundice in extreme cases): bruising due to lack of clotting factors, low platelet count, TPO synthesised in liver
  5. Numbness in extremeties
    6.Neurological problems: build up of toxins makes its way to brain
  6. Thrombocytopenia: low platelet count due to TPO (thrombopoetin) being synthesised in liver
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13
Q

Diagnosis- Biochemistry(5)

A
  1. Liver panel done to assess liver function
  2. Liver enzymes AST:ALT ratio greater than 1 an indication of ARLD
  3. Raised GGT (liver enzyme) linked to ARLD
  4. Low albumin count in liver disease
  5. Increase in bilirubin
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14
Q

Diagnosis - Haematology (2)

A

1. FBC -> PLT levels
2. Clotting screen
3. Serum ferritin (increase with ARLD)

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15
Q

Diagnosis - Histo (1)

A
  1. Biopsy
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16
Q

In a biopsy what would you expect to see at steatosis?

A

Fatty deposits marked by areas of clearing

17
Q

In a biopsy what would you expect to see at fibrosis?

A

Collagen deposition (staining changes)

18
Q

In a biopsy what would you expect to see at cirrhosis?

A

Collagen deposition and changes to vasculature

19
Q

Complications of ARLD (3)

A
  1. Portal hypertension
  2. Ascites
  3. Cancer
20
Q

Portal Hypertension

What is it?

A

Increased pressure within the portal venous system

21
Q

Portal Hypertension

Pathogenesis (4 steps)

A
  1. Cirrhosis and scarring of liver -> architectural changes
  2. Blood forced through smaller blood vessels
  3. Increased resistance
  4. Increased blood pressure
22
Q

Ascites

What is it?

A

A condition where fluid collects in spaces within the abdo (especially the peritoneal cavity)

23
Q

Ascites

Pathogenesis

A
  1. Portal hypertension and vasodilation combined with:
  2. Reduced plasma protein synthesis (esp albumin) and therefore reduced oncotic pressure
24
Q

Ascites

Signs and symptoms (5)

A
  1. Abdo swelling
  2. Abdo discomfort
  3. Weight gain
  4. Early satiety
  5. Shortness of breath
25
Q

Ascites

Complications (2)

A
  1. Abdo infection
  2. Hernia
26
Q

Ascites

Treatment (4)

A
  1. Reduce alcohol intake
  2. Reduce salt and fluid intake
  3. Diuretics
  4. Fluid drains
27
Q

Ascites

Diagnosis (2)

A
  1. Paracentesis: drain with needle. Sent to Micro to rule out infection and to Histo to rule out cancer.
  2. Imaging:MRI and CT
28
Q

Cancer

How is treatment determined

A

By staging and grading with Barcelona staging

29
Q

Cancer

Treatment (3)

A
  1. If HCC localised: surgical excision
  2. If cancer throughout liver but has not spread: transplant
  3. If cancer metastasised: chemo and supportive care
30
Q

Cancer

Prognosis

A
  • Poor but depends on stage of diagnosis
  • Often aggressive due to quick doubling time of hepatocytes
31
Q

Cancer

Diagnosis (4)

A
  1. Signs and symptoms overlap with ARLD
  2. ABnormal liver function tests and clotting times
  3. Histology
  4. Tumour markers: elevated AFP (alpha fetoprotein)