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Gastro + Gen Surg > Alcoholic Liver Disease > Flashcards

Alcoholic Liver Disease Flashcards

1
Q

What are the main functions of the liver?

A

Bile production= aids in absorption of fat + certain vitamins

Fat-soluble vitamin storage + metabolism (A,D,B, K)

Drug metabolism

Plasma protein synthesis i.e. albumin/globulin/protein C/protein S/ clotting factors in intrinsic and extrinsic pathway

Immune response

Bilirubin metabolism

Thyroid hormone function by deiodination of T4->T3

Glycogen storage + gluconeogenesis

Blood detoxification

Iron store

Processes cholesterol

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2
Q

What conditions are included under ALD?

A

Alcoholic fatty liver +/- hepatitis

Alcoholic hepatitis

Cirrhosis

Chronic liver disease (alcoholism is the moat common cause)

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3
Q

What is the pathophysiology of liver cirrhosis due to chronic alcohol abuse?

A

Chronically high intake of alcohol leads to chronic liver injury:
-inflammation due to alcohol making gut leaky which leads to bacteria entering blood and activating the Kupffer cells

  • matrix deposition- oxidative stress causes stellate cell activation i.e. leads to fibrosis
  • necrosis
  • angiogenesis
  • malnutrition leads to impaired regeneration of tissue

I.e. progressive matrix deposition and scar formation leads to fibrosis formation

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4
Q

What are the clinical signs of liver cirrhosis?

A

Leuconychia= white nails -> sign of hypoalbuminaemia

Clubbing

Palmar erythema (effects of oestrogen)

Hyperdynamic circulation= abnormal increased circulating volume
I.e. either presents with collapsing pulse or with bounding pulse

Dupuytrens contracture

Spider naevi

Xanthelasma

Gynaecomastia (effects of oestrogen)

Loss of body hair (look in axilla)-> effects of oestrogen

Hepatomegaly (NOTE: small liver seen in late disease)

Ascites (portal HTN)

Caput Medusa

Splenomegaly (due to increased pressure across the portal venous system)

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5
Q

What signs occur in liver cirrhosis in association with oestrogen and why do they occur?

A

Gynacomastia
Loss of axilla hair
Palmar erythema

Increased production of androstenedione by adrenal glands
Increased aromatisation of androstenedione to oestrogen
Loss of clearance of adrenal androgens by liver
Decreased oestrogen break down by the liver

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6
Q

What are the main complications associated with liver cirrhosis and what are the signs of each?

A

Hepatic failure

  • coagulopathy due to loss of clotting factor sythesis= easy bruising
  • encephalopathy (due to rise in ammonia)= liver flap
  • hypoalbuminaemia -> oedema
  • sepsis
  • hypoglycaemia

Portal hypertension

  • Ascites
  • splenomegaly
  • oesophageal varices
  • portosystemic shunt
  • Caput medusa
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7
Q

Why does portal hypertension occur in liver cirrhosis and how can it be managed?

A

Liver cirrhosis causes obstruction to portal blood flow through the liver which increases the pressure in the hepatic portal system

Beta-blockers= propranolol
-splanchnic vasoconstriction to cause decreases portal and collateral blood flow which decreases portal hypertension

Portosystemic shunts= Transjugular intrahepatic portosystemic shunts
-metal stent guided to intrahepatic branch of portal vein via the internal jugular vein to enable side-to-side shunt
I.e. portal system bypasses the liver and goes straight input systemic circ

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8
Q

What LFT changes are indicative of liver cirrohsis?

A 
Normal or raised bilirubin 
Raised AST and ALT 
Raised gamma GT 
Decreased albumin 
Raised PT/INR
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9
Q

What imaging techniques can be used in liver cirrhosis?

A

Liver ultrasound + duplex

  • hepatomegaly or small liver depending on liver stage
  • splenomegaly
  • focal liver lesions
  • reverse flow in hepatic vein

MRI

  • right posterior hepatic notch= more frequent in alcoholic cirrhosis
  • increased caudate lobe size
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10
Q

Why does ascites occur in liver cirrhosis? (3 main mechanisms)

A

NO, ANP and prostaglandins released in association with liver cirrhosis leads to peripheral vasodilation which decreases effective BV and triggers RAAS
I.e. leads to SALT + WATER RETENTION

PORTAL HYDROSTATIC PRESSURE leads to increased fluid accumulation in peritoneal cavity due to increase hepatic and splanchnic lymph production

LOW SERUM ALBUMIN reduces plasma oncotic pressure which contributes to increased driving force of water out of portal veins

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11
Q

What is the main aim of ascites management? What is the maximum amount of fluid which can be moved in this way?

A

Reduce sodium intake and increase renal sodium excretion= leads to net fluid reabsorption

Reabsorption= 500-700 ml in 24 hrs

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12
Q

What are the methods of ascites management?

A

Fluid restriction <1.5L/day
Low-salt diet= 40-100 mmol/d
Spironolactone= 100mg/24hr
NOTE: furosemide can be used if response to spironolactone is poor

Paracentesis= tense ascites or when diuresis not sufficient in meeting fluid targets

Shunts (TIPS)
-when ascites resistant to other methods of treatment
I.e. decreasing portal hypertension can lead to decrease in ascites

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13
Q

What does patient need to be monitored for when places on furosemide for ascites?

A

Hyponatraemia
Hypokalaemia
Hypovolaemia

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14
Q

A patient suffering from ascites is put onto spironolactone. A recent blood results shows raised creatinine. What has happened?

A

Over-diuresis and hypovolaemia

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15
Q

What condition can patients present with before it progresses to liver cirrhosis? How does a patient present?

A

Alcoholic hepatitis

Raised temp, pulse and resp (TPR) 
D+V
Tender hepatomegaly 
Jaundice 
Ascites
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16
Q

What are signs of severe alcoholic hepatitis?

A

Jaundice
Encephalopathy
Coagulopathy

17
Q

What are the consequences of decreased oestrogen breakdown in liver disease?

A 
Palmar erythema 
Spider Naevi
Gynaecomastia 
Loss of body hair 
Testicular atrophy
18
Q

Why are oesophageal varices associated with liver cirrhosis? What signs are associated with oesophageal varices?

A

The increased portal hypertension leads to increased pressure in the veins of the oesophagus which leads to them dilating and forming varices.

Signs:

  • haematemesis= coffee-ground vomit
  • melena- black tarry stool
  • collapse
  • anaemia
  • abdo pain
19
Q

If patient has been admitted for ALD then they will experience alcohol withdrawal secondary to admission. What are the signs ? How can alcohol withdrawal be managed?

A

Signs:

  • increase pulse
  • decreased BP
  • tremor
  • fits
  • hallucinations

Management:
-use CIWA- Ar to score patient on withdrawal symptoms and inform management
-1st 3 days= chlordiazepoxide (10-50mg/6h)
-IV high dose B1
NOTE: need to plan weaning regime over 5-7days
I.e. sedative and hypnotic medication in benzos class

20
Q

What are the possible cause of chronic liver disease?

A

Alcoholic liver disease
Non-alcoholic fatty liver disease
Cirrhosis

21
Q

What is the progression of hepatic injury due to chronic excessive alcohol consumption?

A

Develop alcoholic fatty liver
-alcohol metabolism leads to fat deposition in liver which causes cells to become swollen with fat but not damaged i.e. steatosis

Alcoholic hepatitis
-prolonged period of inflammation

Alcoholic cirrhosis= final stages of ALD
-scar tissue formation due to matrix deposition

22
Q

What would the bloods of someone with ALD show?

A

Raised MCV= due to alcohol suppressing bone marrow function leading to production of large immature RBC
Elevated ALT + AST + GGT
Low albumin
Increased PT/INR = clotting factors effected

23
Q

What scans can be done for ALD?

A

USS= can show fatty liver i.e. echogenicity

- can do “fibroscan” as part of USS to assess for cirrhosis by sending through high frequency waves

24
Q

How can ALD be managed?

A

CONSERVATIVE:
-Encourage alcohol cessation= need to stop completely
Eg can refer to alcohol specialist nurse

-Nutritional support:
-Thiamine (B1)especially to prevent
Wenricke-Korsaffs syndrome as complication
E.g. Pabrinex= B1 replacement (alcohol prevents B1 absorption)

  • Steroids can be used for alcoholic hepatitis
  • Treat complications= portal hypertension, oesophageal varices, ascites, anaemia (associated with alcohol)

Refer to liver transplant (must be 3 months clear of any alcohol consumption)

25
Q

How does the presentation of alcohol withdrawal change depending on time since last drink?

A 
6-12hrs= tremors, sweating, cravings, headache, anxiety 
12-24hrs= hallucinations 
24-48hrs= seizures 
48-72hrs= delirium tremens
26
Q

Why does alcohol withdrawal lead to delirium tremens?

A

With alcohol:

  • GABA receptors stimulated
  • glutamate receptors inhibited

With chronic alcohol use:
-body compensates for chronically high alcohol levels by down regulating GABA receptors and up-regulating glutamate receptors

Withdrawal of alcohol:
-GABA underfunction and glutamate over functions leading to excessive excitatory activity
I.e. acute confusion, severe agitation, tachycardia, hypertension, tremor, ataxia, arrythmias

27
Q

What is Wenricke-Korsakoff syndrome and what are the 2 different stages? How can it be prevented?

A

Occurs with alcohol excess due to decreased absorption or intake of vitamin B1/thiamine

Wenrickes encephalopathy = medical emergency

  • confusion
  • oculomotor disturbances
  • ataxia

Korsakoff-syndrome = damage to mammillary bodies

  • retrograde and antegrade memory loss
  • behavioural changes

Pabrinex (B1 replacement)

28
Q

Alcohol can severely impact the gut. What other conditions are people with high intact of alcohol at risk of developing?

A

Gastritis

Pancreatitis

Ulcers

GORD

Malnutrition

Anaemia

Oesophageal cancers

Gastro + Gen Surg (45 decks)

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