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Gastrointestinal System > Lecture 5.2: Diseases of the Liver and Pancreas > Flashcards

Lecture 5.2: Diseases of the Liver and Pancreas Flashcards

1
Q

What part of the abdomen is the liver located?

A
  • RUQ
  • Right Hyperchondrium
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2
Q

Functions of the Liver (7)

A
  • Bile production
  • Carbohydrate, protein and lipid metabolism
  • Protein synthesis
  • Vitamin D synthesis
  • Detoxification
  • Vitamin and mineral storage
  • Phagocytosis
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3
Q

Types Liver Function Tests? (3)

A
  • Hepatocellular damage
  • Cholestasis (bile ducts)
  • Synthetic function
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4
Q

What LFTs test for Hepatocellular damage? (2)

A
  • Aminotransferases (ALT/AST)
  • γ-Glutamyl transpeptidase (γ-GT/GGT)
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5
Q

What LFTs test for Cholestasis (bile ducts)? (2)

A
  • Bilirubin
  • Alkaline phosphatase (ALP)
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6
Q

What LFTs test for synthetic function? (3)

A
  • Albumin
  • Prothrombin time (clotting)
  • Glucose
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7
Q

What is Jaundice?

A
  • Yellow pigmentation of the skin and sclera
  • Caused by accumulation of bilirubin in tissue
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8
Q

Why does Jaundice happen?

A

Normal metabolism of bilirubin disrupted (including uptake, transport, conjugation and excretion)

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9
Q

What are the 3 ways Jaundice is classifed?

A
  • Prehepatic (haemolytic)
  • Hepatic (parenchymal)
  • Post hepatic (cholestatic)
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10
Q

When is Bilirubin produced?

A

Breakdown product of RBCs

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11
Q

How is bilirubin normally processed? (5 Steps)

A
  • Unconjugated bilirubin bound to albumin in blood
  • Bilirubin conjugated in liver
  • Excreted in bile into duodenum
  • De-conjugated into urobilinogen
  • Urobilinogen oxidised to form urobilin and stercobilin
    → faeces
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12
Q

What is Pre-Hepatic Jaundice?

A
  • Excessive haemolysis
  • Liver unable to cope with excess bilirubin
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13
Q

Lab findings in Pre-Hepatic Jaundice (3)

A
  • Unconjugated hyperbilirubinaemia
  • Reticulocytosis
  • Anaemia
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14
Q

Causes of Pre-Hepatic Jaundice: Inherited (6)

A
  • Red cell membrane defects (thalassemia)
  • Haemoglobinopathies
  • Metabolic defects
  • Congenital hyperbilirubinaemias
  • Hereditary spherocytosis
  • Sickle Cell Disease
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15
Q

Causes of Pre-Hepatic Jaundice: Acquired (6)

A
  • Immune
  • Mechanical
  • Acquired membrane defects
  • Infections (malaria)
  • Drugs
  • Burns
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16
Q

What is Hepatocellular Jaundice?

A
  • Deranged hepatocyte function
  • Cell necrosis→ inabilty to metabolise or excrete
    bilirubin
  • Element of cholestasis
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17
Q

Lab findings in Hepatocellular Jaundice (4)

A
  • Mixed unconjugated & conjugated
    hyperbilirubinaemia
  • Increased liver enzymes (AST/ALT) reflecting liver
    damage
  • Normal/Increased ALP (cholestasis (swollen cells))
  • Abnormal clotting
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18
Q

Causes of Hepatocellular Jaundice: Inherited (3/5)

A
  • Congenital hyperbilirubinaemias
    • Gilbert’s syndrome (common)
    • Crigler-Najjar syndrome (rare)
    • Dubin-Johnson syndrome (rare)
  • Wilson’s Disease
  • Autoimmune hepatitis
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19
Q

Causes of Hepatocellular Jaundice: Acquired (6)

A
  • Hepatic inflammation
  • Alcohol
  • Drugs (i.e. paracetamol)
  • Cirrhosis
  • Hepatic tumours
  • Haemochromotosis
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20
Q

What is Post-Hepatic/Cholestatic/Obstructive Jaundice?

A
  • Obstruction of biliary system
    • Intrahepatic
    • Extrahepatic
  • Passage of conjugated bilirubin blocked
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21
Q

Lab findings in Post-Hepatic Jaundice? (6)

A
  • Conjugated hyperbilirubinaemia
  • Bilirubin in urine (dark)
  • Pale stools
  • No urobilinogen in urine (no bilirubin enters bowel
    and so is not converted to urobilinogen)
  • Increased canalicular enzymes (ALP)
  • Normal/increased liver enzymes (ALT and AST)
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22
Q

Causes of Post-Hepatic Jaundice: Extrahepatic (obstruction distal to bile canaliculi) (3/7)

A
  • Gallstones
    • Biliary stricture
  • Carcinoma
    • Head of pancreas
    • Ampulla
    • Cholangiocarcinoma (bile duct)
    • Portal hepatis lymph nodes
    • Liver metastases
  • Pancreatitis
    • Sclerosing cholangitis
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23
Q

Causes of Post-Hepatic Jaundice: Intrahepatic (hepatocyte swelling)

A
  • Hepatitis
  • Drugs
  • Cirrhosis
  • Primary biliary cirrhosis
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24
Q

What is Courvoisier’s Law?

A

In the presence of a non-tender palpable gallbladder,
painless jaundice is unlikely to be caused by
gallstones

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25
Q

Gallstones formed over a long period of time result in…?

A

A shrunken fibrotic gallbladder

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26
Q

What is Hepatitis?

A

Inflammation of the Liver

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27
Q

Lab findings in acute hepatocyte breakdown (2)

A
  • Aminotransferase release (AST/ALT)
  • Jaundice
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28
Q

Lab findings in prolonged/chronic hepatocyte damage (3)

A
  • Synthetic failure
  • Decreased albumin
  • Decreased clotting factors
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29
Q

Causes of Hepatitis (7)

A
  • Infections- viral
  • Toxins
  • Alcohol
  • Drugs
  • Wilsons Disease
  • Haemochromatosis
  • Autoimmune
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30
Q

How is Hepatitis A spread? It is acute of chronic?

A
  • Faecal-oral route
  • Usually acute
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31
Q

How is Hepatitis B spread? It is acute of chronic?

A
  • Blood/Body fluids/vertical spread
  • Acute and chronic
  • May progress to cirrhosis
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32
Q

How is Hepatitis C spread? It is acute of chronic?

A
  • Blood spread
  • 50% chronic liver disease
  • 30% cirrhosis
  • 5% hepatocellular carcinoma
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33
Q

How is Hepatitis D spread?

A

Hep B co-infection

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34
Q

How is Hepatitis E spread? It is acute of chronic?

A
  • Faecal-oral
  • Usually acute
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35
Q

What is Alcoholic Liver Disease?

A

Liver damage caused by excess alcohol intake

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36
Q

Pathology of Alcoholic Liver Disease (3)

A
  • Fatty change
  • Alcoholic hepatitis
  • Cirrhosis
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37
Q

Complications of Alcoholic Liver Disease (6)

A
  • Hepatocellular carcinoma
  • Liver failure
  • Wernicke-Korsakoff syndrome
  • Encephalopathy
  • Dementia
  • Epilepsy
38
Q

What is Liver Cirrhosis?

A
  • Liver cell necrosis → nodular regeneration and fibrosis
  • Increased resistance to blood flow
  • Deranged liver function
39
Q

How much of liver parenchyma can be destroyed before any clinical signs present?

A

80-90%

40
Q

Causes of Liver Cirrhosis (7)

A
  • Alcohol
  • Hepatitis B or C
  • Non-alcoholic fatty liver disease
  • Primary biliary cirrhosis
  • Autoimmune hepatitis
  • Haemochromatosis
  • Wilson’s disease
41
Q

Clinical Features of Liver Cirrhosis

A
  • Liver dysfunction
  • Jaundice
  • Anaemia
  • Bruising
  • Palmar erythema
  • Dupuytren’s contracture
  • Portal hypertenision
  • Spontaneous bacterial peritonitis
42
Q

Investigations for Liver Cirrhosis (6)

A
  • →/↑ALT/AST
  • ↑ALP
  • ↑Bilirubin
  • ↓albumin
  • Deranged clotting
  • ↓ Na
43
Q

Management of Liver Cirrhosis (3)

A
  • Stop drinking
  • Treat complications
  • Transplantation
44
Q

Signs and Symptoms of Liver Disease (9)

A
  • Hepatic Flap
  • Clubbing
  • Leukonychia
  • Koilonychia
  • Jaundice
  • Gynacomastia
  • Dupuytren’s Contracture
  • Odema
  • Spider Naevi
45
Q

What is Portal Hypertension?

A

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

46
Q

Causes of Portal Hypertension (3)

A
  • Obstruction of portal vein
  • Obstruction of flow within liver
  • Cirrhosis
47
Q

Clinical Manifestations of Portal Hypertension (5)

A
  • Splenomegaly
  • Ascites
  • Spider Naevi
  • Caput medusa
  • Oesophageal/rectal varices
48
Q

What is stored in the gallbladder?

A
  • Liver produces bile
  • Stored in gallbladder
49
Q

Pathological Processes in the Gallbladder and Biliary Tree (4)

A
  • Obstruction
  • Infection
  • Inflammation
  • Neoplasia
50
Q

Risk Factors for Gallstones (Cholelithiasis): 5 F’s

A

Fair
Fat
Fertile
Female
Forty

51
Q

Risk Factors for Gallstones (Cholelithiasis) (6)

A
  • Increasing age
  • Positive family history
  • Sudden weight loss - eg, after obesity surgery
  • Loss of bile salts - eg, ileal resection, terminal ileitis
  • Diabetes
  • Oral contraception
52
Q

Types of Gallstones

A
  • Mixed (80%, Cholesterol with calcium & bile pigment)
  • Pure cholesterol (10%, usually solitar, up to 5cm)
  • Pigment stones/bilirubin stones (10%, calcium
    bilirubinate, multiple, small and black)
53
Q

What percentage of gallstones are radio-opaque?

A

~10% are radio-opaque

54
Q

What percentage of gallstones are asymptomatic?

A

~70%

55
Q

Complications of Gallstones (13): Name 5

A
  • Biliary colic
  • Impaction of stone in cystic duct
  • Gallbladder contraction
  • Cholecystitis
  • RUQ pain & fever
  • Sepsis
  • Local peritonism
  • Raised white cell count
  • Gallbladder mass
  • Recurrent acute attacks may become chronic
  • Ascending cholangitis
  • Obstructive jaundice
  • Acute pancreatitis
56
Q

How does pain due to gallstones present?

A
  • Sudden onset of epigastric/RUQ pain
  • Radiates to back
  • Lasts 15 minutes up to 24 hours
  • Resolves spontaneously or with analgesics
  • Associated nausea and vomiting
57
Q

Management of (Complications of) Gallstones (4)

A
  • Analgesia
  • NBM
  • IV Antibiotics and fluids
  • Surgery – laparoscopic cholecystectomy
58
Q

What is Charcot’s Triad?

A

The manifestation of biliary obstruction with:
* Upper Abdominal Pain
* Fever
* Jaundice

59
Q

What is Ascending Cholangitis?

A
  • A life-threatening condition caused by an ascending
    bacterial infection of the biliary tree
  • Inflammation/infection of the CBD
  • Bacteria ascend from CBD junction with the
    duodenum
  • Bile duct is already partially obstructed by gallstones
60
Q

Management of Ascending Cholangitis (3)

A
  • Resuscitate
  • IV broad spectrum antibiotics
  • Surgery – endoscopic drainage of CBD
61
Q

What are the Contents of the Triangle of Calot?

A
  • Right Hepatic artery
  • Cystic artery
  • Any aberrant/accessory ducts
62
Q

Functions of the Pancreas: Endocrine

A
  • Insulin
  • Glucagon
  • Somatostatin
63
Q

Functions of the Pancreas: Exocrine

A
  • Fluid (HCO3)
  • Enzymes
  • Proteolytic, amylase, lipolytic
64
Q

What is Pancreatitis?

A
  • Inflammation of the pancreas
  • Inflammatory process caused by effects of enzymes
    released from pancreatic acini
65
Q

What changes occur in the Pancreas due to Acute Pancreatitis (3)

A
  • Oedema
  • Haemorrhage
  • Necrosis
66
Q

What changes occur in the Pancreas due to Chronic Pancreatitis (5)

A
  • Fibrosis
  • Calcification
  • Loss of acini
  • Duct stenosis
  • Parenchymal destruction
67
Q

Causes of Acute Pancreatitis: GET SMASHED

A
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion bite
  • Hyperlipidaemia
  • ERCP/Iatrogenic
  • Drugs
68
Q

What causes 80% of Acute Pancreatitis cases? (2)

A
  • Gallstones
  • Ethanol
69
Q

Pathogenesis/Clinical Presentations of Pancreatitis (6)

A
  • Duct obstruction (from juice & bile reflux)
  • Acinar damage (from reflux or drugs)
  • Tissue destruction (via proteases)
  • Fat necrosis (via lipases)
  • Blood vessel destruction (via elastases)
  • Enzymes digest pancreatic tissue
70
Q

How does pain caused by acute pancreatitis present?

A
  • Sudden severe epigastric pain
  • Penetrates to the back
  • Vomiting
  • Steadily decrease over 72 hours
71
Q

What is Cullen’s Sign?

A

Superficial bruising in the subcutaneous fat around the umbilicus

72
Q

What is Grey Turners Sign?

A

An uncommon subcutaneous manifestation of intra-abdominal pathology that manifests as ecchymosis or discolouration of the flanks

73
Q

What conditions is Cullen’s Sign seen in? (7)

A
  • Acute pancreatitis
  • Rectus sheath hematoma
  • Splenic rupture
  • Perforated ulcer
  • Intra-abdominal cancer
  • Ruptured ectopic pregnancy
  • Complication of anticoagulation
74
Q

What condition is Grey Turners Sign seen in?

A

Severe acute necrotizing pancreatitis

75
Q

Treatment of Acute Pancreatitis

A
  • Supportive – NG tube and IVI (drip and suck)
  • Fluid balance
76
Q

What biochemical changes occur in acute pancreatitis? (4)

A
  • ↑Amylase
  • ↓Ca2+
  • ↑Glucose
  • ↑ALP/Bilirubin
77
Q

What are the clinical presentations of chronic pancreatitis? (5)

A
  • Pain
  • Malabsorption
  • Steatorrhoea, wt loss
  • DM
  • Jaundice
78
Q

When does pancreatic carcinoma present?

A
  • Late presentation
  • Early metastases
  • Poor survival rates
79
Q

Risk Factors for Pancreatic Carcinoma (7)

A
  • Smoking
  • Over 60
  • High Fat Diet
  • Alcohol
  • Chronic Pancreatitis
  • Diabetes
  • Family History
80
Q

Clinical Features Pancreatic Carcinoma (9)

A
  • Initially symptomless/vague
  • Painless progressive obstructive jaundice
  • Nausea
  • Vomiting
  • Pain
  • Weight Loss
  • Carcinomatosis
  • Malabsorption
  • Diabetes
81
Q

How many pancreatic carcinomas are found in the head of the pancreas?

A

70% in head of pancreas

82
Q

What is the most common type of pancreatic carcinoma? What percentage of pancreatic carcinomas does it make up?

A
  • Ductal adenocarcinoma
  • 90%
83
Q

What effect does pancreatic cancer invading the pancreatic head have on surrounding structures? (3)

A
  • Can compress and obstruct the bile duct,
  • Can compress/obstruct hepatopancreatic ampulla
  • If cancer invades posteriorly, it can invade/block
    portal venous confluence of splenic vein + SMV
84
Q

Treatment of Pancreatic Carcinoma

A
  • Surgery (only 10-20%)
  • Chemotherapy
  • Palliative
85
Q

Prognosis of Pancreatic Carcinoma

A
  • 5th cause of cancer death in UK
  • 5-year survival rate less than 5%
86
Q

What is Gilbert’s Syndrome?

A
  • Inherited condition
  • The faulty gene means that bilirubin isn’t passed into
    bile at the normal rate
  • Thus bilirubin build up in blood
87
Q

Name 5 causes of obstruction to flow of bile from the liver and gallbladder

A
  • CBD gallstones
  • Carcinoma
  • Pancreatic Pseudocyst
  • Biliary Stricture
  • Sclerosing Cholangitis
88
Q

What is HUS?

A
  • Haemolytic Uremic Syndrome
  • A kidney condition that happens when red blood cells
    are destroyed and block the kidneys’ filtering system
89
Q

Symptoms of HUS?

A
  • Vomiting
  • Bloody Diarrhea
  • Stomach Pain
  • Fever
  • Chills
  • Headache
90
Q

What causes HUS?

A

In most cases, HUS occurs after a severe bowel infection with certain toxic strains of the bacteria called E. coli. It may also occur in response to certain medicines, but this is rare.

91
Q

Treatment of HUS (6)

A
  • Plasma Exchange
  • Treatment of high blood pressure
  • Maintaining specific levels of fluids and salts
  • Blood transfusions
  • Kidney dialysis
  • Medicine

Gastrointestinal System (22 decks)

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