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13. Gastrointestinal > 7. Liver, Gallbladder, and Pancreas 2 > Flashcards

7. Liver, Gallbladder, and Pancreas 2 Flashcards

1
Q

What are the range of toxins that the GI tract may be exposed to?

A

Chemical, bacteria, viruses, protozoa, nematodes (roundworms), cestodes (tapeworms), trematodes (flukes).

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2
Q

What are the two categories of GI tract defences to toxins?

A

Innate (physical and cellular) and adaptive).

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3
Q

What are the physical innate defences of the GI tract?

A

Sight/smell - if food looks or smells bad, it normally isn’t eaten. Memory - if food tastes bad, you don’t eat it next time. Saliva is pH 7.0 and contains lysozymes, lactoperoxidase, complement, IgA and polymorphs so washes toxins into stomach. Stomach acid has a low pH to kill most bacteria and viruses. Small intestine secretions like bile, proteolytic enzymes, lack of nutrients, shedding of epithelial cells. Colonic mucus protects epithelium from its contents. Anaerobic environment in small bowel and colon. Peristalsis and segmentation to get toxins through and out of body.

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4
Q

What are the cellular innate defences of the GI tract?

A

Neutrophils, macrophages - Kupffer cells in liver, natural killer cells, tissue mast cells, esoinophils - for parasitic infections.

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5
Q

What are Kuppfer cells?

A

Specialised macrophages in the liver.

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6
Q

What is the venous drainage of the GI tract?

A

It passes through the liver via the hepatic portal system before returning to the systemic circulation.

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7
Q

What are the adaptive defences of the GI tract?

A

B lymphocytes produce antibodies against extracellular microbes, T lymphocytes directed against intracellular organisms, and lymphatic tissues MALT and GALT in nodules - tonsils, Peyer’s patches, and appendix.

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8
Q

What is mucosal associated lymphoid tissue (MALT) called in the GI tract?

A

Gut associated lymphoid tissue (GALT).

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9
Q

What are the three locations where GALT is nodular?

A

Tonsils, Peyer’s patches, and appendix.

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10
Q

What is xerostomia?

A

Reduced salivary flow from severe illness and/or dehydration.

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11
Q

What is the consequence of xerostomia?

A

Microbial overgrowth in the mouth and dental cavities.

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12
Q

What staphylococcus aureus infection can results from xerostomia?

A

Parotitis - salivery gland infections.

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13
Q

What is achlorhydria?

A

Absent or low gastric acid production.

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14
Q

What can cause achlorhydria?

A

Pernicious anaemia, drugs like H2 antagonists of PPIs.

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15
Q

What are patients with achlorhydria more susceptible to?

A

Shigellosis, cholera, and salmonella infections.

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16
Q

What are patients in hospital taking PPIs at an increased risk of acquiring?

A

Clostridium difficile.

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17
Q

Which organisms are resistant to gastric acid?

A

Mycobacterium tuberulosis, enteroviruses (like hepatitis A, polio, and coxsackie), and helicobacter pylori.

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18
Q

How can helicobacter pylori survive in the stomach with gastric acid?

A

It produces urease, which acts on urea to produce a protective cloud of ammonia.

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19
Q

What do mast cell granules contain?

A

Histamine.

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20
Q

What is the results of mast cell recruitment in the GI tract?

A

Histamine is released causing vasodilation and increased capillary permeability which leads to massive fluid loss.

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21
Q

How quickly can fluid be lost with cholera?

A

1 litre lost per hour.

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22
Q

What is the mortality of untreated cholera?

A

60%.

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23
Q

What may be mistaken for appendicitis in children?

A

Mesenteric adenitis as it causes right iliac fossa pain in children.

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24
Q

What causes mesenteric adenitis?

A

Adenovirus/ coxsackie virus.

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25
Q

What causes inflamed Peyer’s patches in the terminal ileum?

A

Typhoid fever.

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26
Q

What is the result of perforation of inflamed Peyer’s patches in the terminal ileum?

A

Death.

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27
Q

What is a common cause of appendicits?

A

Lymphoid hyperplasia at the appendix base leading to an obstructed outflow.

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28
Q

When is purulent appendicitis more common?

A

During epidemics of chickenpox in children.

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29
Q

What can obstruct the appendix other than lymphoid hyperplasia at the appendix base?

A

Faecolith - calcified faecal matter, a worm.

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30
Q

What can intestinal/hepatic ischaemia be due to?

A

Arterial disease, systemic hypotension, or intestinal venous thrombosis.

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31
Q

What can the result of intestinal or hepatic ischaemia be?

A

Overwhelmin sepsis and rapid death within a few hours.

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32
Q

What does liver failure increase susceptibility to?

A

Infections, toxins, drugs, and hormones.

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33
Q

How can liver failure results in hepatic encephalopathy?

A

Increased blood ammonia from failure of the urea cycle. Ammonia from colonic bacteria and deamination of amino acids can cause it.

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34
Q

What are the causes of liver failure?

A

Viral hepatitis, alcohol, drugs (paracetamol, halothane), industrial solvents, mushroom poisoning.

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35
Q

How does the worldwide cause of liver failure from the UK cause?

A

Worldwide - viral hepatitis.

UK - alcohol.

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36
Q

What can portosystemic shunting lead to?

A

Oesophageal varices, haemorrhoids, and caput medusa.

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37
Q

What are the sequelae of hepatic fibrosis?

A

Portal venous hypertension, then portosystemic shunting and therefore toxin shunting.

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38
Q

What are bile products?

A

Excretory products.

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39
Q

What is the most common bile pigment?

A

Bilirubin.

40
Q

What is bilirubin from?

A

Product of haemoglobin breakdown.

41
Q

How is jaundice caused?

A

If bilirubin can’t be excreted it accumulated in the blood -jaundice.

42
Q

What happens to bilirubin from the liver onwards?

A

Conjugated in the liver, then secreted in bile to excreted in faeces.

43
Q

What is the notable hormone that the liver breaks down?

A

Insulin.

44
Q

What is the most abundant plasma protein?

A

Albumin.

45
Q

What is albumin essential?

A

Maintaining the oncotic pressure needed for proper distribution of body fluids.

46
Q

What are the coagulation factors that the liver produces?

A

Coagulation factors: I (fibrinogen), II (prothrombin), V, VII, IX, X, XI. Protein C, S and antithrombin.

47
Q

What is thrombopoietin?

A

A glycoprotein hormones that regulates the production of platelets by bone marrow.

48
Q

How does the liver affect amino acids?

A

It transaminises them.

49
Q

What is ALT and AST presence indicative of?

A

Liver damage, as damaged hepatocytes ruptured membranes allow aminotransferases into the blood stream.

50
Q

What causes bilirubin plasma concentration to rise?

A

If the bile ducts are unable to excrete bilirubin.

51
Q

What causes alkaline phosphatase to rise?

A

Enzymes in the cell lining the liver’s biliary ducts make it so rises with obstruction.

52
Q

When are albumin levels reduced?

A

In chronic liver disease.

53
Q

What does prothrombin time measure?

A

The clotting tendency of the blood.

54
Q

What is the visible results of hyperbilirubinaemia?

A

Yellowish pigmentation of the skin, conjunctival membranes over the scleae and other mucus membranes.

55
Q

At what level does jaundice become clinically detectable?

A

> 40umol/L (normal is 22umol/L).

56
Q

What is pre-hepatic jaudice?

A

Excessive bilirubin production, usually due to an increased breakdown of red blood cells so liver is unable to cope with excess bilirubin.

57
Q

What are the lab findings of pre-hepatic jaundice?

A

Unconjugated hyperbilirubinaemia, reticulocytosis, anaemia, increased LDH, decreased haptoglobin.

58
Q

What are the inherited causes of pre-hepatic jaundice?

A

Red cell membrane defects, haemoglobin abnormalities, metabolic defects.

59
Q

What are the congenital hyperbilirubinaemias causes of pre-hepatic jaundice?

A

Gilbert’s syndrome, Crigler-Najjar syndrome (rare), Dublin-Johnson syndrome (rare).

60
Q

What are the acquired causes of pre-hepatic jaundice?

A

Immune, mechanical, acquired membrane defects, infections, drugs, burns.

61
Q

What is hepatic jaundice?

A

Reduced capacity of liver cells to secrete conjugated bilirubin into the blood.

62
Q

What are the lab findings of hepatic jaundice?

A

Mixed unconjugated and conjugated hyperbilirubinaemia, increased liver enzymes, abnormal clotting.

63
Q

What are the congenital causes of hepatic jaundice?

A

Gilbert’s syndrome, Crigler-Najjar syndrome.

64
Q

What are the hepatic inflammation causes of hepatic jaundice?

A

Viral - hepatitis A, B, C, and E, Epstein Barr virus. Autoimmune hepatitis, alcohol, haemochromotosis, Wilson’s disease.

65
Q

What is a drug that can cause hepatic jaundice?

A

Paracetamol.

66
Q

What can cause cirrhosis that can lead to hepatic jaundice?

A

Alcohol, chronic hepatitis, metabolic disorders.

67
Q

What are the hepatic tumours that can cause hepatic jaundice?

A

Hepatocellular carcinoma, metastases.

68
Q

What is post-hepatic jaundice?

A

Obstruction to the drainage of bile, causing a back up of bile acids into the liver. Can be intrahepatic or extrahepatic. The passage of bilirubin is blocked.

69
Q

What are the lab findings of post-hepatic jaundice?

A

Conjugate hyperbilirubinaemia, bilirubin in urine (dark), increased canalicular enzymes (ALP), increased liver enzymes (ALT/AST).

70
Q

What are the intrahepatic causes of post-hepatic jaundice?

A

Hepatitis, drugs, cirrhosis, primary biliary colic.

71
Q

What are the extrahepatic causes of post-hepatic jaundice?

A

Gallstone/ biliary stricture, carcinoma (of head of pancreas, ampulla, bile duct, porta hepatis lymph nodes, or liver metastases) pancreatitis, sclerosing cholangitis.

72
Q

What is the pathology of fatty liver disease?

A

Alcohol metabolism generates NADH from NAD+, NADH induces fatty synthesis and decreased NAD+ means decreased fatty acid oxidation. There is accumulation of fatty acids in the liver so TAGs accumulate - fatty liver.

73
Q

What is alcoholic hepatitis?

A

Inflammation of hepatocytes.

74
Q

What is cirrhosis?

A

Liver cell necrosis followed by nodular regeneration and fibrosis, resulting in increased resistance to blood flow and deranged liver function.

75
Q

What are the causes of cirrhosis of the liver?

A

Alcohol, Wilson’s disease, a1-antitrypsin deficiency, biliary colic, haemochromotosis, hepatitis B or C, autoimmune hepatitis.

76
Q

What are the clinical features of cirrhosis of the liver?

A

Liver dysfunction, jaundice, anaemia, bruising, palmar erythema, Dupuytren’s contracture.

77
Q

What are the investigation results of cirrhosis of the liver?

A

Increased ALT/AST, increased ALP, increased bilirubin, decreased albumin, deranged clotting.

78
Q

What is the management of liver cirrhosis?

A

Stopping drinking, treating complications, and transplantation.

79
Q

What is portal hypertension defined as?

A

Portal venous pressure above 20mmHg.

80
Q

What can cause portal hypertension?

A

Obstruction of the portal vein (congenial, thrombosis or extrinsic compression), or obstruction of flow within the liver (cirrhosis, hepatoportal sclerosis, Schistosomiases, sarcoidosis).

81
Q

How does portal hypertension cause ascites?

A

High pressure means blood is backed up in the abdomen. The increase in hydrostatic pressure means less fluid is reabsorbed into blood vessels at ends of capillary beds. If linked with liver damage, oncotic pressure may be reduced inside vessels too.

82
Q

How does portal hypertension cause splenomegaly?

A

Subsequent increase in blood pressure in the spleen.

83
Q

What are the sequelae of portal hypertension on porto-systemic anastamoses?

A

Oesophageal varices, rectal varices, caput medusae.

84
Q

What is the porto-systemic anastomosis involved in oesophageal varices?

A

Left gastric -> azygous/oesophageal.

85
Q

What is the porto-systemic anastomosis involved in rectal varices?

A

Superior rectal -> inferior rectal.

86
Q

What is the porto-systemic anastomosis involed in caput medusae?

A

Paraumbilical -> small epigastric of abdominal wall.

87
Q

Where are bile acids stored?

A

In the gall bladder.

88
Q

How is more bile acid stored in the small gall bladder?

A

By concentration, transport of salt and water across gall bladder epithelium.

89
Q

What is the risk of the gall bladder concentrating bile acid?

A

Risk of precipitation leading to gall stones.

90
Q

What are the complications of gallstones?

A

Very painful biliary colic if in the neck of the gall bladder or biliary tree. Can cause obstruction -> inflammation (cholecystitis) and infection.

91
Q

Why is biliary colic pain worse after eating?

A

Secretion of cholecystokinin causes the gallbladder to contract.

92
Q

What is pancreatitis caused by generally?

A

Inflammatory process from the effects of enzymes released from pancreatic acini.

93
Q

What are the acute features of pancreatitis?

A

Oedema, haemorrhage, necrosis, severe pain, vomiting, dehydration, shock, decrease Ca2+, increased amylase, glycaemia, ALP, and bilirubin.

94
Q

What are the chronic features of pancreatitis?

A

Fibrosis, calcification, pain, malabsorption, jaundice.

95
Q

What are the causes of pancreatitis?

A

GET SMASHED: gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion bite, hyperlipidaemia, ERCP/iatrogenic, drugs.

96
Q

What is the most common form of pancreatic carcinoma?

A

Ductal adenocarcinoma.

97
Q

What is the clinical presentation of pancreatic carcinomas?

A

Initially symptomless, but then lots of symptoms at once: obstructive jaundice, pain, vomiting, malabsorption, diabetes.

13. Gastrointestinal (17 decks)

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