7. Liver, Gallbladder, and Pancreas 2 Flashcards
What are the range of toxins that the GI tract may be exposed to?
Chemical, bacteria, viruses, protozoa, nematodes (roundworms), cestodes (tapeworms), trematodes (flukes).
What are the two categories of GI tract defences to toxins?
Innate (physical and cellular) and adaptive).
What are the physical innate defences of the GI tract?
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.
What are the cellular innate defences of the GI tract?
Neutrophils, macrophages - Kupffer cells in liver, natural killer cells, tissue mast cells, esoinophils - for parasitic infections.
What are Kuppfer cells?
Specialised macrophages in the liver.
What is the venous drainage of the GI tract?
It passes through the liver via the hepatic portal system before returning to the systemic circulation.
What are the adaptive defences of the GI tract?
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.
What is mucosal associated lymphoid tissue (MALT) called in the GI tract?
Gut associated lymphoid tissue (GALT).
What are the three locations where GALT is nodular?
Tonsils, Peyer’s patches, and appendix.
What is xerostomia?
Reduced salivary flow from severe illness and/or dehydration.
What is the consequence of xerostomia?
Microbial overgrowth in the mouth and dental cavities.
What staphylococcus aureus infection can results from xerostomia?
Parotitis - salivery gland infections.
What is achlorhydria?
Absent or low gastric acid production.
What can cause achlorhydria?
Pernicious anaemia, drugs like H2 antagonists of PPIs.
What are patients with achlorhydria more susceptible to?
Shigellosis, cholera, and salmonella infections.
What are patients in hospital taking PPIs at an increased risk of acquiring?
Clostridium difficile.
Which organisms are resistant to gastric acid?
Mycobacterium tuberulosis, enteroviruses (like hepatitis A, polio, and coxsackie), and helicobacter pylori.
How can helicobacter pylori survive in the stomach with gastric acid?
It produces urease, which acts on urea to produce a protective cloud of ammonia.
What do mast cell granules contain?
Histamine.
What is the results of mast cell recruitment in the GI tract?
Histamine is released causing vasodilation and increased capillary permeability which leads to massive fluid loss.
How quickly can fluid be lost with cholera?
1 litre lost per hour.
What is the mortality of untreated cholera?
60%.
What may be mistaken for appendicitis in children?
Mesenteric adenitis as it causes right iliac fossa pain in children.
What causes mesenteric adenitis?
Adenovirus/ coxsackie virus.
What causes inflamed Peyer’s patches in the terminal ileum?
Typhoid fever.
What is the result of perforation of inflamed Peyer’s patches in the terminal ileum?
Death.
What is a common cause of appendicits?
Lymphoid hyperplasia at the appendix base leading to an obstructed outflow.
When is purulent appendicitis more common?
During epidemics of chickenpox in children.
What can obstruct the appendix other than lymphoid hyperplasia at the appendix base?
Faecolith - calcified faecal matter, a worm.
What can intestinal/hepatic ischaemia be due to?
Arterial disease, systemic hypotension, or intestinal venous thrombosis.
What can the result of intestinal or hepatic ischaemia be?
Overwhelmin sepsis and rapid death within a few hours.
What does liver failure increase susceptibility to?
Infections, toxins, drugs, and hormones.
How can liver failure results in hepatic encephalopathy?
Increased blood ammonia from failure of the urea cycle. Ammonia from colonic bacteria and deamination of amino acids can cause it.
What are the causes of liver failure?
Viral hepatitis, alcohol, drugs (paracetamol, halothane), industrial solvents, mushroom poisoning.
How does the worldwide cause of liver failure from the UK cause?
Worldwide - viral hepatitis.
UK - alcohol.
What can portosystemic shunting lead to?
Oesophageal varices, haemorrhoids, and caput medusa.
What are the sequelae of hepatic fibrosis?
Portal venous hypertension, then portosystemic shunting and therefore toxin shunting.
What are bile products?
Excretory products.