Gastro-intestinal Flashcards
Describe the pathway for absorption of folate
Folate is taken in from dietary sources, stored as folate polyglutamate. Folate deconjugase in the stomach converts it into folate monoglutamate, which is absorbed via specific folate carriers in the proximal small intestine.
Describe the pathway for absorption of cobalamin
Cobalamin is taken from dietary sources, where it is released from food via stomach acid. R protein binds to cobalamin, where it is cleaved in the duodenum. Free cobalamin then binds to intrinsic factor. Intrinsic factor, produced by the exocrine pancreas, and small percentage of the gastric mucosa in dogs. Cobalamin and intrinsic factor complex then binds to receptors found on enterocytes in ileum, bound to transcobalamin which transport it to cells.
What diseases can cause folate and cobalamin deficiencies?
Cobalamin deficiency - caused by EPI/ exocrine pancreatic disease, distal ileal disease, diffuse small intestinal disease if ileum involved, and bacterial dysbiosis (cobalamin competition with bacteria).
Folate deficiency - caused by proximal small intestinal disease, or diffuse small intestinal disease affecting the proximal intestine. Bacterial dysbiosis can lead to INCREASED folate, due to bacterial production.
Describe the pathophysigology of development of acute canine pancreatitis
Co-localisation theory:
Mansfield C 2012 - co-localisation theory. Apical block at the cell membrane which prevents lysozymes from excreting enzymes. Will get accumulation of trypsinogen and lysosome at the membrane surface. Combination of the granules then results in activation of trypsin, leading to direct recruitment of neutrophils into the cells, resulting in a pro-necrosis state. IL 8 leads to further recruitment and adherence of neutrophils.
What the risk factors associated with development of canine acute pancreatitis?
Hyperlipoproteinaemia
Obesity
Drugs/ toxins - azathioprine, chlorthiazide, KBr, Zinc, sulfonamides
Hypercalcaemia
Duct obstruction
Duodenal/ biliary reflux
Pancreatic ischaemia/ trauma/ injury
Endocrinopathies - hyperadrenocorticism, diabetes mellitus, hypothyroidism
Idiopathic
What are the potential haematology and biochemistry changes that may occur with acute canine pancreatitis?
Haematology
- Erythrocytosis or anaemia (secondary to dehydration or inflammation)
- Leukopaenia or leukocytosis (secondary to left shifting and acute inflammatory response)
- Thrombocytopaenia (may be precipitating DIC)
Biochemistry
- Azotaemia (prerenal due to dehydration and reduced GFR, and renal due to concurrent AKI)
- Hypoglycaemia or hyperglycaemia (transient due to hyperglucagonaemia and stress hormone release, or permanent due to diabetes mellitus)
- Liver enzyme elevations (concurrent liver damage from toxin released into portal circulation)
- Hyperbilirubinaemia (secondary to inflammation and compression of biliary canniculi compression, or secondary fatty hepatic change)
- Hyponatraemia, hypochloridaemia (fluid shifting and dehydration)
- Hypercalcaemia (unknown mechanism)
- Hypertriglyceridaemia - transient inhibition of lipoprotein lipase, resulting in increased triglycerides
- Hyperamylasaemia - release by pancreas
- Hyperlipasaemia - release by pancreas
Discuss serum amylase use in diagnosis of acute canine pancreatitis
Serum amylase is produced by duodenum, stomach and pancreas.
Cleared by renal tubules, and Kupffer cells in liver.
Peaks about 24-48 hours after onset of pancreatitis, and can take 8-14 days to return to normal
Sensitivity = 68-72%
Specificity = 57-77%
Discuss serum lipase use in diagnosis of acute canine pancreatitis
Lipase produced by pancreas as well as stomach
Excreted renally
Increases within 24 hours, and peaks 3-5 days after pancreatitis
Sensitivity = 60-75%
Specificity = 57-77%
Other diseases that can increase serum lipase are:
- Gastritis
- Peritonitis
- Enteritis
- Some hepatopathies
- Some neoplasias (pancreatic, hepatic carcinomas, pancreatic ductal carcinomas, gastrointestinal lymphosarcomas)
- bowel obstruction (unknown mechanism)
- corticosteroid administration (unknown mechanism)
Discuss use of specific pancreatic lipase (CPL) for diagnosis of acute canine pancreatitis and acute feline pancreatitis
Measurement of serum lipase which has only been derived from the pancreas
Sensitivity and specificity in dogs:
- 81% and 96%
Sensitivity and specificity in cats:
- 67% and 91%
Tends not to be affected by gastritis, oral prednisolone administration or GFR changes
List the possible causes of vomiting in small animals
Primary GIT
- Adverse food reactions/ dietary intolerance/ dietary indiscretions
- Chronic enteropathy/ IBD
- Post-operative ileus
- Hypomotility disorder
- Dysautonomia
- Gastro-intestinal neoplasia
- Gastro-intestinal infections - parasites, bacterial or viral gastro-enteritis
- Partial or complete gastro-intestinal obstructions
- Food bloat/ food stomach dilation
- Gastritis
Extra-GIT
- Hepatic insufficiency/ hepatic disease
- Cholecystitis
- Splenitis
- Pancreatitis
- Diabetic keto-acidosis
- Hypercalcaemia
- Extra-GIT neoplasia
- Hypoadrenocorticism
- Drug related
- Uraemia/ renal insufficiency
- Pyometra
- CNS disorders - increased ICP
- Sialadenosis/ sialadenitis
- Peritonitis
- Hyperthyroidism
- Endotoxaemia
- Acid/base disturbances
