5.2- Diseases of the Liver and Pancreas Flashcards

1
Q

What 3 tests check liver function?

A
  • Hepatocellular damage
  • aminotransferases (ALT/AST)
  • gamma glutamyl transpeptidase (y-GT)
  • Cholestasis ( bile ducts)
  • bilirubin
  • alkaline phosphatase; suggests cholestasis or bone breakdown
  • Synthetic function (APG)
  • albumin
  • prothrombin time (clotting)
  • glucose
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2
Q

What is jaundice?

A

yellow pigmentation of the skin and sclera caused by accumulation of bilirubin in tissue

  • clinically detectable when bilirubin>40umol/L
  • normal range <22 umol/L
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3
Q

How do you classify jaundice?

A

1) Prehepatic ( haemolytic)
2) Hepatic (parenchymal)
3) Post-hepatic (cholestatic); backup of bilirubin in blood

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4
Q

What is the cause of jaundice?

A

disruption of the normal metabolism of bilirubin

May arise from any:

  • Excessive bilirubin production because of increased haemolysis ( pre-hepatic)
  • Reduced capacity of liver cells to secrete unconjugated bilirubin into blood; hepatic/intra-hepatic
  • obstruction to drainage of bile, causing backup of bilirubin into liver ; post-hepatic
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5
Q

What is bilirubin?

A
  • breakdown product of RBCs
  • unconjugated biliirubin is bound to albumin in blood
  • bilirubin is conjugated in the liver ie bound to glucoronic acid+becomes water soluble
  • excreted in bile into duodenum
  • de-conjugated into urobilinogen
  • urobilinogen oxidised to form urobilin and stercobilin, which go into faeces
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6
Q

Once formed, what happens to urobilinogen?

A
  • it gets oxidised in the duodenum to form urobilin and stercobilin, which leave in the stool
  • trace of urobilinogen also gets reabsorbed into the eneterohepatic circulation:

and then re-excreted in bile

-also goes to kidneys and colour them yellow

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7
Q

What is pre-hepatic jaundice?

A
  • because of excessive haemolysis due to anything
  • liver is unable to cope with excess bilirubin

LAB FINDINGS:

1) Unconjugated hyperbilirubinaemia: (because bilirubin is unconjugated before it gets to the liver)

ie high amounts, is pre-hepatic jaundice

2) Reticulocytosis: immature RBCs (pre-hepatic jaundice)
3) Anaemia

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8
Q

What are the causes of pre-hepatic jaundice?

A

ie anything that causes haemolysis

  • Inherited:
  • RBC membrane defects
  • Haemoglobinopathies eg sickle cell
  • metabolic defects
  • Congenital hyperbilirubinaemias

-Gilbert’s syndrome- common a lack of function in the enzyme that conjugates bilirubin

  • Crigler-Najjar syndrome-rare
  • Dubin Johnson syndrome-rare
  • Acquired:
  • immune
  • mechanical
  • infections
  • drugs eg NSAIDS, cephalosporins, nitrafurantoin
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9
Q

What is hepatocellular jaundice?

A

ie hepatic/ intra-hepatic jaundice

  • deranged hepatocyte function
  • cell necrosis→inability to metabolise or excrete bilirubin
  • happens w cholestasis ie slow sloppy movement of bile
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10
Q

What are the lab findings of hepatocellular jaundice?

A
  • mix of unconjugated and conjugated hyperbilirubinaemia
  • increased liver enzymes ie AST/ALT, reflects liver damage
  • same or increased ALP; causes cholestasis and swollen cells (alkaline phosphatase)
  • abnormal clotting
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11
Q

Name 9 causes of hepatocellular jaundice?

A
  1. Congenital
  2. Hepatic inflammation
  3. Autoimmune hepatitis
  4. Alcohol
  5. Drugs eg paracetamol
  6. Cirrhosis
  7. Hepatic tumours
  8. Haemochromatosis-depositions of Fe
  9. Wilson’s disease- depositions of Cu
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12
Q

What is post-hepatic/cholestatic/jaundice?

(OBSTRUCTIVE JAUNDICE)

A
  • Obstruction of biliary system; can be intrahepatic or extrahepatic
  • passage of conjugated bilirubin locked
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13
Q

What are the lab findings of post-hepatic/obstructive jaundice?

A
  • conjugated hyperbilirubeinaemia
  • bilirubin in urine ie dark ( bc of backup through liver intoblood; gets excreted into urine instead)
  • pale stools ie steatorrhoea
  • no urobilinogen in urine ie no bilirubin enters bowel so is not converted to urobilinogen
  • increased canalicular enzymes ie ALP ( indicator of cholestasis/blockage of bile)
  • raised ALT and AST bc of backing into liver
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14
Q

What are the causes of post-hepatic jaundice? ( Intrahepatic and Extrahepatic)

A

INTRAHEPATIC:hepatocyte swelling (HDCP)

  • hepatitis
  • drugs
  • cirrhosis
  • primary biliary cirrhosis

EXTRAHEPATIC: obstruction distal to bile canaliculi (GBC)

  • gallstones
  • biliary structure
  • carcinoma in:
  • head of pancreas
  • ampulla
  • cholangiocarcinoma ie bile duct
  • porta hepatis lymph nodes
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15
Q

What is Courvoisier’s law for post-hepatic jaundice?

A
  • in the presence of a non-tender palpable gallbladder, painless jaundice is unlikely to be caused by gallstones
  • GB is often more enlarged when there is biliary obstruction over a shorter period of time eg malignancy

-tender GB seen in:

  • acute cholecystitis; tender and distended w a mucocele or empyema related to gallstones
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16
Q

Recap: What are the 3 types of jaundice?

A

HOT LIVER

Pre-hepatic- Haemolytic

Hepatic- Obstruction

Post hepatic- cholestatic ie tumour

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17
Q

What is hepatitis?

A
  • inflammation of the liver*
  • can be acute or chronic
  • Acute hepatocyte breakdown; causes Aminotransferase release (AST/ALT) and jaundice
  • Prolonged/chronic damage:
  • synthetic failure*
  • low albumin*
  • low clotting factors*
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18
Q

What are the causes of Hepatitis?

A
  • infections-viral
  • Toxins ie alcohol/haemochromatosis/ Wilson’s disease/drugs
  • Autoimmune
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19
Q

What is viral hepatitis and what are the types?

A
  • Hepatitis A:

​-goes in via the faecal-oral route ie contaminated water+ usually acute

6F’s: faeces, flies fluid, field, fluids, fingers, food

  • Hepatitis B:
  • blood/body flluids/ vertical spread eg cervical transmission
  • acute and chronic; may progress to cirrhosis
  • Hepatitis C:
  • blood spread
  • involves chronic liver disease, cirrhosis and hepatocellular carcinoma
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20
Q

State the pathology and complications of alcoholic liver disease

A
  • Pathology:

fatty change

alcoholic hepatitis

cirrhosis

  • Complications: (6)
  • hepatocelluar carcinoma
  • liver failure bc of cirrhosis
  • Wernicke-Korsakoff syndrome
  • Dementia
  • Encephalopathy
  • Epilepsy
21
Q

What is liver cirrhosis?

A
  • liver cell necrosis, causes nodular regeneration and fibrosis
  • increased resistance to blood flow
  • deranged liver function
22
Q

What are the causes of liver cirrhosis?

A
  • alcohol
  • hepatits B/C
  • non-alcoholic fatty liver disease
  • primary biliary cirrhosis
  • autoimmune hepatitis
  • haemachromatosis
  • Wilson’s disease
23
Q

Name some clinical features of liver cirrhosis.

A

-LIVER DYSFUNCTION:

  • jaundice
  • anaemia
  • Dupuytren’s contracture
  • palmar erythema
  • bruising
  • Portal hypertension
  • Spontaneous bacterial peritonitis
24
Q

What is defined as portal hypertension?

A
  • portal venous pressure> 12 mmHg due to intrahepatic or extrahepatic portal venous compression/ occlusion

CAUSED BY:

  • Obstruction of the portal vein; blood backs up and opens up channels to other places
  • Obstruction of flow withun the liver ie cirrhosis
25
Q

What investigations do you conduct for liver cirrhosis? (6)

A
  • check for normal raised ALT/AST
  • increased ALP
  • increased bilirubin
  • decreased bilirubin
  • deranged clotting
  • check for low Na
26
Q

How do you manage liver cirrhosis? (STT)

A
  • Stop drinking
  • Treat compliations
  • Transplantation
27
Q

Name 5 clinical manifestations of portal hypertension?

A
  • splenomegaly
  • spider naevi
  • ascites
  • oesophageal/ rectal varices
  • caput medusa
28
Q

What are the different ducts near the liver and GB?

A

GB responsible for storage and passage of bile from liver to duodenum

Pathological processes which cano happen (OIIN)

  • Obstruction
  • Inflammation
  • Infection
  • Neoplasia
29
Q

What are gallstones?

A

cholelithiasis

(fair, fat, fertile, female and forty)

30
Q

What are the risk factors for getting gallstones? (6)

A
  • increasing age
  • positive family history
  • sudden weight loss eg after obesity surgery
  • loss of bile saltsl eg ileal resectiom, terminal ileitis
  • oral contraception
  • diabetes
31
Q

What are the 3 types of gallstones?

A
  • MIXED: cholesterol w calcium and bile pigments
  • PURE CHOLESTEROL: usually solitary, up to 5cm
  • PIGMENT STONES( BILIRUBIN STONES): calcium bilirubinate, multiple, small and black
32
Q

Name 5 complications of gallstones?

A
  • Biliary colic
  • Cholecystitis
  • Ascending cholangitis
  • Obstructive jaundice
  • Acute pancreatitis
33
Q

What is biliary colic?

A
  • happens in cystic duct; impaction of stone in the cystic duct
  • gallbladder contraction happens to try and get rid of obstruction
  • sudden onset of epigastric/ RUQ pain that radiates to the back
  • lasts from 15 mins-24 hours; resolves spontaneously or w analgesics
  • associated nausea and vomiting
34
Q

What is cholecystitis?

A

inflammation of the gallbladder

  • impaction of stone in cystic duct
  • RUQ pain and fever
  • sepsis
  • local peritonism
  • raised WBC count
  • gall bladder mass
  • raised attacks may become chronic
35
Q

How is cholecystitis managed?

A
  • analagesia
  • NBM- nil by mouth
  • IV antibiotics and fluids
  • surgery: laparoscopic cholecystectomy
36
Q

What is ascending cholangitis?

A
  • inflammation/infection of the common bile duct
  • bacteria ascend from the CBD junction with the duodenum
  • bile duct is already partially obstructed by gallstones
  • LIFE THREATENING
37
Q

How does ascending cholangitis present and how can it be managed?

A

Presents with:

Charcot’s triad:

-RUQ pain

-Obstructive jaundice

-Fever, shock, confusion

Manage with:

  • resuscitate
  • IV broad spectrum antibiotics
  • surgery; Endoscopic drainage of common bile duct
38
Q

What is pancreatitis?

A
  • inflammation of the pacnreas
  • inflammatory process caused by effects of enzymes released from pancreatic acini
  • can be acute or chronic
39
Q

Differentiate between acute and chronic pancreatitis?

A

Acute pancreatitis: -oedema, haemorrhage, necrosis

(OHN)

Chronic pancreatitis: fibrosis and calcification (FC)

40
Q

What are the causes of acute pancreatitis?

GET SMASHED

A
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion bite
  • Hyperlipidaemia
  • ERCP/ iatrogenic
  • Drugs
41
Q

What is the pathogenesis of acute pancreatitis?

A
  • Duct obstruction; juice and bile reflux
  • Acinar damage; from reflux or drugs
  • Protease leaking out from tissue destruction
  • Lipase from fat necrosis
  • Elastase from blood vessel destruction
42
Q

What are the clinical signs of acute pancreatitis?

A
  • sudden severe epigastric pain
  • penetrates to the back
  • vomiting
  • steadily decreases over 72 hours
43
Q

How is acute pancreatitis treated?

A
  • supportive; drip and suck; IV fluids and NG tube
  • fluid balance
44
Q

What biochemical changes do you see in acute pancreatitis?

A
  • high amylase
  • low calcium
  • high glucose
  • high ALP/ bilirubin
45
Q

What is chronic pancreatitis?

A
  • parenchymal destruction, fibrosis, loss of acini and duct stenosis
  • Chronic alcoholism; CF, inherited, biliary disease
46
Q

What are the clinical signs of chronic pancreatitis?

A
  • pain
  • malabsorption; weight loss, steatorrhoea
  • jaundice
  • DM
47
Q

What are the risk factors of pancreatic carcinoma?

A
  • smoking
  • over 60 yrs
  • high fat diet
  • alcohol
  • chronic pancreatitis
  • DM
  • FHx
48
Q

What are the clinical features of pancreatic carcinoma?

A

late presentation, early metastases and poor survival rates

-normally a ductal adenocarcinoma, mostly in the head of pancreas

  • initially asymptomatic
  • painless progressive obstructive jaundice
  • nausea and vomiting

Symptoms:

  • pain
  • weight loss
  • malabsorption
  • diabetes
  • carcinomatosis
49
Q

How is pancreatic carcinoma managed?

A
  • surgery
  • chemotherapy
  • palliative