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GI (Semester 4) > 5.2 Liver and pancreatic disease > Flashcards

5.2 Liver and pancreatic disease Flashcards

1
Q

What are the main functions of the liver?

A
  • Bile production
  • Carbohydrate, protein and lipid metabolism
  • Protein synthesis
  • Vitamin D synthesis
  • Detoxification
  • Vitamin and mineral storage
  • Phagocytosis
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2
Q

What liver function tests would indicate hepatocellular damage? (2)

A
  • Aminotransferases (ALT/AST)

* γ-Glutamyl transpeptidase (γ-GT)

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3
Q

What liver function tests would indicate cholestasis (bile ducts)? (2)

A
  • Bilirubin

* Alkaline phosphatase

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4
Q

What liver function tests would indicate synthetic function? (3)

A
  • Albumin
  • Prothrombin time (clotting)
  • Glucose
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5
Q

What is jaundice?

What is the main cause?

A

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

Caused by the disruption of normal bilirubin metabolism eg. uptake, transport, conjugation and/or excretion

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6
Q

What are the normal levels of bilirubin?

What levels of bilirubin are indicative of jaundice?

A

Normal range <22 umol/L

Clinically detectable when bilirubin >40 umol/L

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7
Q

What are the 3 ways in which we can classify the type of jaundice?

A

1) Prehepatic (haemolytic)
2) Hepatic (hepatocellular)
3) Post hepatic (obstructive)

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8
Q

What are the products of haemoglobin breakdown?

How are these metabolised in the liver?

What are the 3 fates of the final product following oxidation by bacteria?

A

Haemoglobin breaks down to heme (hame➞biliverdin ➞biliruben) and globin (breaks into amino acids)

1) biliruben entering liver is unconjugated
2) In liver: bilirubin is conjugated to glucuronic
acid by UDP-glucuronosyltransferase
3) this forms the conjugated version (water soluble) which is released in bile into duodenum and small intestine
5) In the small intestine, it is oxidised by bacteria to urobilinogen

Urobilinogen can do 3 things:

1) some is reabsorbed
2) some is excreted via kidney as urobilin
3) remaining turned into stercobilinogen and furthur oxidised into stercobilin which is excreted in the feces

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9
Q

What give urine its yellow colour and faeces its brown colour?

A

urine: yellow because of urobilin
faeces: brown because of stercobilin

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10
Q

Explain the relationship between bilirubin and bile

A

Bile salts aid in digestion and Bilirubin is the main pigment in bile

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11
Q

How is the unconjugated bilirubin transported in the blood?

A

bound to albumin (it then reaches liver)

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12
Q

How is pre-hepatic jaundice (haemolytic) characterised?

A

Characterised by excessive haemolysis ➞ liver unable to cope with excess bilirubin

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13
Q

What 3 lab findings would indicate pre-hepatic jaundice and why?

A

1) Unconjugated hyperbilirubinaemia ➞ excess RBC break down, so increased unconjugated bilirubin entering liver
2) Reticulocytosis ➞ hemolysis results in increased production of reticulocytes by bone marrow (reticulocytes -= immature RBCs)
3) Anaemia ➞ due to excess haemolysis

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14
Q

Give 3 causes of pre-hepatic jaundice for the following:

Inherited
Aquired
Congenital hyperbilirubinaemias

A

Inherited: RBC membrane defects, haemoglobinopathies, metabolic defects

Aquired: Infection, drugs, mechanical

Congenital hyperbilirubinaemias (in order of most-least common)

1) Gilberts syndrome ➞ decreased activity of UGT
2) Crugler-Najjar syndrome ➞ absent UGT
3) Dubin-Johnson syndrome ➞ un-excretable bilirubin

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15
Q

How is hepatocellular jaundice (parenchymal) characterised?

A

Characterised by deranged hepatocyte function ➞ cell necrosis which causes inabilty to metabolise or excrete bilirubin

+ there is an element of cholestasis (reduction or stoppage of bile flow)

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16
Q

What 4 lab findings would indicate hepatocellular jaundice and why?

A

1) Mixed unconjugated and conjugated hyperbilirubinaemia ➞ some hepatocytes still normal
2) raised AST/ALT ➞ due to liver damage
3) normal or raised ALP ➞ indicates cholestasis due to swollen cells
4) Abnormal clotting ➞ some hepatocytes cant produce clotting factors

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17
Q

Give 4 causes of hepatocellular jaundice

A

1) Drugs (eg. paracetamol)
2) Cirrhosis
3) Hepatic tumours
4) congenital

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18
Q

How is post-hepatic jaundice (obstructive) characterised?

How can it be sub-classified and what does this mean?

A

Characterised by obstruction of the biliary system ➞ passage of conjugated bilirubin is blocked

Sub-classification:
Intrahepatic ➞ hepatocyte swelling
Extrahepatic ➞ obstruction distal to bile canaliculi

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19
Q

What 5 lab findings would indicate post-hepatic jaundice and why?

A

1) Conjugated hyperbilirubinaemia ➞ conjugation still occurs in liver
2) Dark urine (bilirubin in urine) ➞ obstruction causes conjugated bilirubin in liver to be excreted in kidney in that form (not oxidised to urobilin), giving the dark colour
3) Pale stools/”clay stools” ➞ obstruction means bilirubin cant flow into small intestine and be converted in stercobilinogen, so no brown in faeces
4) raised canalicular enzymes (ALP)
5) normal or raised liver enzymes (ALT and AST)

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20
Q

Give 4 causes of post-hepatic jaundice for Intrahepatic AND Extrahepatic

A

Intrahepatic:

1) Hepatitis
2) Drugs
3) Cirrhosis
4) Primary biliary cirrhosis

Extrahepatic:

1) Gallstones
2) Biliary stricture
3) Carcinoma
4) Pancreatitis
5) Sclerosing cholangitis

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21
Q

Give 4 types of Carcinoma that can lead to post-hepatic jaundice (include locations)

A
  • Head of pancreas
  • Ampulla
  • Cholangiocarcinoma (bile duct)
  • Porta hepatis lymph nodes
  • Liver metastases
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22
Q

What is Courvoisier’s law in reference to post-hepatic jaundice

A

States that: ‘in the presence of a non-tender palpable

gallbladder, painless jaundice is unlikely to be caused by gallstones’.

23
Q

Why is a non-tender palpable gallbladder unlikely to be gallstones? (Courvoisier’s law)

Give an example

A

As gallstones are formed over a long period of time it would result in a shrunken fibrotic gallbladder.

An enlarged gallbladder is more indicative of pathologies causing biliary obstruction which occurs over shorter periods of time

Eg. a tender gallbladder may be seen with acute cholecystitis or a tender and distended gallbladder may be seen with a mucocele or empyema related to gallstones

24
Q

What is hepatitis?

List 3 causes

A

inflammation of the liver

Causes:

1) Infections- viral
2) Toxins (Alcohol, drugs, wilsons, haemochromatosis)
3) Autoimmune

25
Q

List 2 findings that would be indicative of ACUTE hepatocyte breakdown

A

1) Aminotransferase release (AST/ALT)

2) Jaundice

26
Q

List 3 findings that would be indicative of prolonged/ chronic hepatocyte damage

A

1) Synthetic failure
2) decreased albumin
3) decreased clotting factors

27
Q

What are the 3 types of viral hepatitis?

List how each is spread and whether it is acute or chronic

A

1) Hepatitis A
• Faecal-oral (shellfish)
• Usually acute

2) Hepatitis B
• Blood/Body fluids/vertical spread
• Acute and chronic ➞ may progress to cirrhosis

3) Hepatitis C
• Blood spread
• 50% chronic liver disease, 30% cirrhosis, 5% hepatocellular carcinoma

28
Q

What are the 3 stages of Alcoholic liver disease

A

1) Fatty liver
2) Alcoholic hepatitis
3) Cirrhosis

29
Q

List 6 complications of Alcoholic liver disease

A

1) Hepatocellular carcinoma
2) Liver failure
3) Wernicke-Korsakoff syndrome
4) Encephalopathy
5) Dementia
6) Epilepsy

30
Q

What is seen in liver cirrhosis and give 2 ways this effects function

What is the difficulty with diagnosis?

A

Liver cell necrosis which leads to nodular regeneration and fibrosis

Results in increased resistance to blood flow and deranged liver function. Final outcome is often liver diseases

Early diagnosis is difficult as clinical signs are usually only seen after 80-90% of liver parenchyma has already been destroyed

31
Q

Give 3 causes of liver cirrhosis

A

1) Alchol
2) Hepatitis B or C
3) Non-alcoholic fatty liver disease
4) Primary biliary cirrhosis

32
Q

Give 4 signs/symptoms of liver dysfunction + 2 other clinical features

A
  • Jaundice
  • Anaemia
  • Bruising
  • Palmar erythema
  • Dupuytren’s contracture

+ Portal hypertension and spontaneous bacterial peritonitis

33
Q

List 6 lab findings that would indicate liver cirrhosis

A

1) normal to raised ALT/AST
2) increased ALP
3) increased bilirubin
4) decreased albumin
5) deranged clotting
6) decreased Na

34
Q

list 3 main principals of treatment/management of liver cirrhosis

A

1) Stop drinking alcohol
2) Treat complications
3) Transplantation

35
Q

What defines portal hypertension and what is this a result of?

Give the 2 main causes of this

A

Portal venous pressure >12 mmHg, due to intrahepatic or extrahepatic portal venous compression or occlusion

Causes:

1) Obstruction of portal vein
2) Obstruction of flow within liver (eg. cirrhosis)

36
Q

What are the visible clinical signs of portal hypertension? (5)

A

1) splenomegaly
2) ascites
3) spider naevi
4) caput medusa
5) oesophageal/rectal varices

37
Q

Give 4 pathological processes that may cause diseases of the gallbladder and/or biliary tree

What is the main consequence of this

A

1) obstruction
2) Infection
3) Inflammation
4) neoplasia

We cannot store or and deliver bile from liver to duodenum, which is necessary for the absorption of fats

38
Q

What is the clinical name for gallstones?

What are the 5 MAIN risk factors + 2 others (hint 5F’s)

A

Gallstones = Cholelithiasis

Risk factors: ‘Fair, fat, fertile, female and forty’

Others incl: Increasing age, FHx, diabetes, OCP

39
Q

Give the 3 main types of gallstones + their composition and appearance

A

1) Mixed 80% (most common) ➞ cholesterol with calcium and bile pigment
2) Pure cholesterol 10% ➞ usually solitary and upto 5cm
3) Pigment stones (bilirubin stones) 10% ➞ calcium bilirubinate, usually multiple that are small and black

40
Q

What are 3 major complications of gallstones?

List 2 others

A

1) Billary colic
2) Cholecystitis
3) Ascending cholangitis

Others:
• obstructive jaundice
• acute pancreatitis

41
Q

What is Billary colic?

Describe the pain a patient would present with and list 2 associated symptoms

How would you treat?

A

Occurs when a gall stone blocks the cystic duct (recurrent acute attacks may become chronic)

Presentation: when gallbladder contracts patient feels sudden onset severe epigastric/RUQ pain that radiates to the back and lasts 15 minutes - 24 hours

Associated symptoms: nausea and vomiting

Treatment: usually resolves spontaneously but If it doesn’t analgesics can be used

42
Q

What is Cholecystitis and how would this present?

How would you treat and what are 2 serious consequences if untreated?

A

Inflammation of the gallbladder (often followed by infection) due to Irritation of the biliary tract by stone

Presentation: RUQ pain and fever

Treatment: analgesia, IV antibiotics + fluids, laparoscopic cholecystectomy

If untreated can progress to: sepsis, local peritonism, raised WCC, gallbladder mass

43
Q

What is Ascending cholangitis?

Describe the pain a patient would present with

Why Is this a medical emergency and how would you treat?

A

Inflammation/infection of the CBD due to bacteria ascending from duodenum

Presentation: Charcot’s triad (RUQ pain, Jaundice, Fever)

Infection can become life threatening because the CBD is already partially obstructed by gallstones

Treatment: resuscitate, IV broad spectrum antibiotics, endoscopic drainage of CBD

44
Q

What are the endocrine and exocrine functions of the pancreas?

A

Endocrine: Insulin, glucagon, somatostatin

Exocrine: HCO3 and enzymes (protease, amylase, lipase etc…)

45
Q

List the 4 close anatomical relations of the pancreas

A

1) duodenum
2) common bile duct
3) portal vein
4) coeliac trunk

46
Q

What is pancreatitis and what causes it?

A

Inflammation of the pancreas ➞ caused by effects of

enzymes released from pancreatic acini

47
Q

What is seen in acute vs chronic pancreatitis?

A

Acute: oedema, haemorrhage, necrosis

Chronic: fibrosis, calcification

48
Q

Give the 2 MAIN causes of pancreatitis + 4 other causes

GET SMASHED

A

Main: 80% of cases

1) gallstones
2) ethanol

Other: trauma, steroids, mumps, autoimmune, scorpion bite, hyperlipidaemia, ERCP/Iatrogenic, drugs

49
Q

What is the Pathogenesis of pancreatitis? (why does it develop) (5)

A

1) Duct obstruction ➞ juice and bile reflux
2) Acinar damage ➞ from reflux or drugs
3) Protease ➞ tissue destruction
4) Lipase ➞ fat necrosis
5) Elastase ➞blood vessel destruction

Enzymes digest pancreatic tissue!!

50
Q

What is the clinical presentation of ACUTE pancreatitis?

What are the biochemical changes (lab findings)?

How would you treat

A

Presentation: sudden severe epigastric pain that penetrates to the back a/w with vomiting (steadily decreases over 72 hours)

Biochemical changes (lab findings)
↑Amylase
↓Ca2+
↑Glucose
↑ALP/Bilirubin

Treatment: supportive - fluid balance

51
Q

What does CHRONIC pancreatitis result in? (4)

Give 4 causes

What Is the clinical presentation?

A

Results in: parenchymal destruction, fibrosis, loss of acini and duct stenosis

Causes: chronic alcoholism, cystic fibrosis, inherited conditions, biliary disease

Clinical presentation:
• pain
• malabsorption ➞ steatorrhoea and weight loss
• diabetes mellitus ➞ damage to endocrine pancreas
• jaundice

52
Q

What is the prognosis of Pancreatic carcinoma and why?

Which is the most common type and what is the most location

Give 6 risk factors

A

Poor survival rates b/c of late presentation and early metastases (5th cause of cancer death in UK)

90% ductal adenocarcinoma and 70% in head of pancreas

Risk factors: smoking and alcohol, over 60, high fat diet, chronic pancreatitis, diabetes, FHx

53
Q

Describe the progression that would be seen in Pancreatic carcinomas

A

1) Initially symptomless/vague
2) painless progressive obstructive jaundice
3) nausea and vomiting
4) severe progression to: pain, weight loss, carcinomatosis (multiple carcinomas), malabsorption

54
Q

How do you treat Pancreatic carcinomas?

A
  • Surgery (only 10-20%)
  • Chemotherapy
  • Palliative

GI (Semester 4) (19 decks)

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