Conditions Flashcards

1
Q

What is delirium tremens?

A

Acute confusional state which results when someone who drinks excess alcohol daily, suddenly stops drinking. Untreated it results in seizures and even death.

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2
Q

What is biliary obstruction?

A

Due to gallstones and is usually accompanied by repeated biliary colic and/or attacks of cholangitis (inflammation of bile duct system).
Will present early with painful jaundice and minimal dilation of the bile ducts.

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3
Q

How does carcinoma of head of pancreas or carcinoma of ampulla of vater present?

A

Progressively worsening painless jaundice and marked dilation of biliary tree.

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4
Q

What is hepatic encephalopathy?

A

Changes in the brain that occurs in patients with advanced, acute or chronic liver disease. Liver cannot break down toxins e.g. ammonia so they can build up in blood and enter brain.

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5
Q

Life cycle of bilirubin

A
  • Formed as breakdown of haem
  • Conjugated in liver - water soluble
  • Extricated in the bile
  • Metabolised in gut by bacteria
  • Reabsorbed and excreted in the liver
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6
Q

What is fulminant hepatitis?

A

Acute hepatitis with liver failure
Encephalopathy within 28 days of jaundice
Poor prognosis often needs transplantation

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7
Q

Causes of cirrhosis

A
  • Hazardous alcohol
  • Chronic hepatitis B and C
  • Autoimmune liver disease
  • Haemachromatosis (excess iron)
  • Wilson’s disease (copper toxicity)
  • Chronic obstruction
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8
Q

What causes hepatic encephalopathy?

A

Acute liver failure

Decompensated liver cirrhosis

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9
Q

What does bile contain?

A
  • Bile pigments which are Hb breakdown products

- Bile salts (glyine or taurine) derived from cholesterol

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10
Q

What happens to bilirubin in hepatocytes?

A

It is protein bound, then conjugated to glucoromic acid (controlled by glucuronyl transferase). This causes it to be water-soluble so is excreted in bile.

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11
Q

Breakdown of conjugated bilirubin

A

By bacterial proteases in small intestine to urobilinogen. Some is excreted in faeces but some is reabsorbed via the portal vein and is excreted in the kidneys.

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12
Q

What are the causes of haemolytic jaundice?

A
  • RBC abnormality e.g. sickle cell
  • Can be due to incompatible blood transfusion
  • Drug reaction
  • Hypersplenism
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13
Q

Pathophysiology of haemolytic jaundice

A

Glucuronyl transferase is saturated so liver compensates for increased conjugated bilirubin output so stools are dark.
Excess of unconjugated bilirubin in plasma and it cannot be excreted in urine so little or no bilirubin in urine (not dark urine).

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14
Q

Causes of hepatocellular jaundice

A
  • Congenital
  • Infection (viral hepatitis)
  • Cirrhosis (secondary to alcohol)
  • Cirrhosis (secondary to steatohepatitis (NASH) - damage by inflammatory mediators from fat cells)
  • Damage by toxins or drugs
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15
Q

What happens in acute pancreatitis?

A

Enzymes become activated before leaving pancreas so they attack and digest pancreatic tissue - inflamed pancreas.

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16
Q

Causes of acute pancreatitis

A
  • Alcohol
  • Gallstones
  • Abdominal trauma
  • Medications
  • Infections
  • Tumours
  • Idiopathic
17
Q

How is acute pancreatitis diagnosed?

A
  • Increased amylase and lipase in blood tests

- CT - swollen pancreas

18
Q

What happens in chronic pancreatitis?

A

Inflammation of pancreas causing destruction of pancreatic tissue which affects nutrient absorption.

19
Q

What is used to diagnose chronic pancreatitis?

A
  • US +/- CT
  • MRCP
  • AXR
    Speckled calcification, faecal elastase
20
Q

What is cholecystitis?

A

When gallstones continue to block the biliary duct leading to inflamed gallbladder. The gallbladder irritation causes mucosal linings to release mucus within gallbladder - promotes bacterial growth. Bacteria can spread out causing peritonitis (rebound tenderness).

21
Q

What are the risk factors for developing hepatocellular cancer?

A
  • Hep B worldwide
  • Hep C Europe
  • Alcohol
  • Haemochromatosis
  • Primary Biliary Cirrhosis
  • alpha-1 antitrypsin deficiency