Intro To Intestinal Disease Flashcards
Define digestion
The orderly process by which proteins, fats and carbohydrates are broken down in to absorbable units
What are the two phases of digestion?
- Luminal to start with
- Then at the level of the mucosal/membranous
Define absorption
The process by which products of digestion and vitamins, minerals and water cross the mucosa to enter blood or lymph
What is the role of the mouth in digestion of CHO?
Salivary alpha-amylase begins starch digestion to mainly maltose, some glucose and dextrins
What is the surface area of the SI provided by (3)
- villi
- Microvilli
- Increase SA further = optimising
- brush border
- protective glycocalyx layer
- brush border enzymes
What happens in the luminal phase in the SI?
Starch breakdown continued by pancreatic amylase to maltose…
…cannot yet be absorbed
What happens in the membranous phase in the SI?
Dissacharides to monosaccharides by glucosidase enzymes (maltase, sucrase and lactase) located in intestinal brush border
Monosaccarides transported across intestinal mucosa, what is glucose and maltose limited by the rate of?
Epithelial transport
Monosaccarides transported across intestinal mucosa, what is lactose limited by the rate of?
Rate of hydrolysis
What does CHO active transport require energy from?
Na+K+ATPase (sodium pump)
How does the sodium pump work?
Na+linked glucose transporter. 2 binding sites, 1 for glucose and 1 for sodium.
- Generate gradient
- Transport nutrient
H+linked transporter:
Some dipeptides
How does CHO facilitated trasport work? What is it used for?
Does not require energy but instead uses concentration gradient of substrate to activate pumps
Fructose
Glucose
Mannose
Xylose
Galactose
Fructose
What is the rate of absorption in order?
galactose > glucose > fructose > mannose > xylose
How is protein digested?
Protein first denatured by stomach acid then passes to small intestine
Luminal phase: specific proteases hydrolyse protein to short chain peptides
Membranous phase: hydrolysed further to mainly di/tripeptides but some free amino acids
How are amino acid actively trasported?
Specific membrane proteins then transport across gut wall by secondary active transport (as for CHO)
There is a risk of autolysis by pancreatic proteolytic enzymes. What is the defence mechanism for this?
- inactive enzymes secreted in to the pancreatic duct in zymogen granules
- activation only occurs in the intestinal lumen eg trypsinogen to trypsin
How is lipids transported?
–Micelles transport lipids across enterocyte cell membranes
–Chylomicrons (large lipoprotein complexes) are used for transport in lymphatic circulation
–Short chain tgs absorbed directly
How is lipid digested?
- Emulsification is crucial and depends on bile
- Pancreatic lipase is activated in the intestine
What is EPI?
What are the signs?
–Inadequate secretion of pancreatic enzymes
–Maldigestion
–Steatorrhoea
What does biliary disease cause? (gall stones, cholestatic liver disease, extrahepatic biliary obstruction)
–Failure of emulsification
–Lipase works but unable to solubilise lipids into micelles
–Maldigestion
What is the problem with intestinal mucosal abnormalities?
(inflammation, viral/bacterial infection, neoplastic infiltration).
Malabsorption
What drug inhibits GI lipase and reduces fat absorption? Licensed?
–Orlistat (xenical)- not licensed
- Toxicity studies in dogs
- Predictable adverse effects….
Name a drug that inhbitis microsomal TAG transfer protein? Reduces appetite and FA uptake (2) Is it authoriseed?
–Mitratapide (yarvitan) -no longer authorised
–Dirlotapide (slentrol)-no LONGER AUTHORISED
Is the gut lumen inside or outside the body?
Outside
What is the function of intestinal microflora?
–Complex role of the mucosal immune system
What is the impact of oral antibacterial and diseases on the flora?
Interrupt microflora
What is the role of the portal blood flow?
•Take blood from gut to the liver without having to dilute in the body. It is then cleaned up and processed. Disruption – you end up knowing the impact. PSS which where the PV doesn’t take to the liver and clinically these animal can be severely affected.
What is the role of the ileocaecal valve?
•Between the SI and LI – important to maintain separation here. If you removed thisyouget a lot of problems of dumping SI into the LI = D+
What are the 2 patterns of SI motility, what is the functtion and how do they work?
•Peristalsis
–Reflex response to stretch of the gut wall
–Coordinated
–Oesophagus to rectum
–Influenced by autonomic NS
•Segmentation
–Slows down transit
–Enables mixing of chyme & enzymes (gut contents)
What are the patterns of motility in the colon? What are the functions of this?
•Peristalsis
–Slower rate than in the SI as the colon’s role it to ABSORB WATER (if there isn’t enough time for this you end up with D+)
–Enables time for absorption of
- Approx 90% of the water from intestinal chyme
- Sodium
- Some minerals
–You may not see D+ in bowel disease because the colon may still absorb water. But the SI may be failing to absorb = weight loss
•Segmentation
–Facilitates absorption of water by mixing
What is going on here?
Ileus: direct inhibition of smooth muscle causing a decrease in intestinal motility.
What is going on here in this cat?
Dysautonomia contributing to constipation. Other clinical signs include regurgitation due to megoesophagus secondary to oesophageal motility problems and urine retention. Loose ability of smooth muscle
What are the general clinical signs of intestinal disease? (10)
- Diarrhoea
- Vomiting
- Abdominal pain/discomfort
- Weight loss – chronic, small bowel
- Anorexia
- Flatulence
- Borborygmi
- Constipation
- Tenesmus
- Melaena or haematochezia
How can you differentiate between small and large intestinal diarrhoea?
Define diarrhoea
Passing faeces with:
- Increased volume
- And/or increased frequency
What are the 4 categories of diarrhoea?
- Osmotic
- Secretory
- Inflammatory
- Motility disorder
What is the pathophysiology of osmotic diarrhoea?
–Maldigestion (eg EPI, damage to the brush border)
–Malabsorption (eg mucosal damage, villus atrophy, infiltrative disease such as lymphoma)
What is the pathophysiology of secretory diarrhoea?
–Toxin
–Infection related
What is the pathophysioloogy of inflammatory diarrhoea?
Inflammatory bowel disease (eg adverse food reaction, idiopathic chronic enteropathy)
What do clinical signs of Campylobacter vary with?
The strain of organism
•Organism may be pathogenic to one species but not another
–Risk of reservoirs of pathogens in healthy animals
–Resistance can be innate or acquired
–Stress effects
Name 2 examples of this.
–Campylobacter in a number of wild life and poultry without observable disease.
–E. Coli O157 in cattle
Why should you be careful giving anti-diarrhoea tablets?
Diarrhoea can be productive
How do you initially investigate intestinal disease?
•Signalment
–Consider breed, age
–Individual or herd problem?
–Zoonotic implications?
•Full clinical history
–Background history
–Current illness history
–Review the history if necessary!
•Physical examination
–The GI tract is inaccessible
–Look for
What could anaemia mean with intestinal disease?
Could just be as it is a chronic disease, gi bleeding – iron deficient
What does Polycythaemia mean on haematology with GI disease?
Dehydration
What may an inflammatory leucogram mean on GI disease haematology?
inflammation – does it look like the body is impacted?, infection, parasites, may have a stress response
What may lymphopenia mean on haematology with GI disease?
lymphangiectasia
What may Eosinophilia, lymphocytosis mean on haematology with GI disease?
hypoadenocorticism
On biochemsitry what would you see with:
A) Dehydration?
B) Fluid imbalance?
C) Protein loss in the gut?
A) Hiigh urea, creatinine, total proteins
B) Electrolyte abnormalities
C) Low albumin globulin
On biochemsitry what would you see with:
A) GI bleed
B) Functional liver disease?
C) FIP in in cats?
A) High urea +/- low protein
B) Low urea, low cholesterol, low albuin, low glucose
C) High globulin
On biochemsitry what would you see with:
A) Hypoadrenocorticism?
B) Malabsorption?
A) hyperkalaemia, hyponatraemia
B) low cholesterol +/- albumin
What faecal analysis can we do?
–Swab or sample?
–Think about pathogenic organisms
–Think when you interpret results
What can we look at on faecal parasitology?
–Nematodes
–Cestodes
–Protozoa (intermittent shedding?)
- Giardia – do we need multiple samples?
- Tritrichomonas in cats
What facecal virus tests can we do?
–Parvo SNAP test?
–Coronavirus?
When would abominal radiography be indicated?
- Abdominal pain?
- Vomiting and diarrhoea?
- Weight loss?
- Melaena?
When would you think about doing thoracic radiography?
- Metastatic disease?
- Concurrent oesophageal disease?
what large bowel signs would make us want to conduct a colonoscopy?
–Tenesmus
–Mucus
–Fresh blood
–Increased urgency, small volumes
What type of test rules out disease?
Sensitive
What type of test rules in disease?
Specific
What are the benefits of a gross examination and how do we do this?
Can tell if it looks abnormal or not. Ex. Lap. Is the main way we do this. Gross abnormalities may not be present as the external surface isn’t that useful. Internal surface via endoscopy may help.
When should we biopsy?
Always biopsy, multiple sites- SI, LI and LN
Where may a biopsy give a limited info?
Submucosal mass e.g. bowel tumours – may only give normal muscos as the thing that is wrong is below the mucosa
What is this? How could we treat?
Granuloma gastritis
Preds mend this
What is this and where is it common?
Angular incisa carcinoma
Internal divisions
What is this?
Worm
What is this?
Gi lymphoma
What is this?
Multifocal GI lymphoma
Inflammed
Biopsy may give a neutrophil gastritis and a negative result
So may need to re biopsy
What is this?
Loss of layers
Eosionophilli enteritis
How may you need to manage the consequences of intestinal disease?
Symptomatic treatment
What 5 things (other than fluid) can an animal loose when vomiting and diarrhoeaing?
Na+
K+
Cl-
HCO3-
pH
What is the effect of SI diarrhoea on acid base?
What are the 2 main goals of treatment?
What treatment often causes complications?
- common cause of metabolic acidosis
- loss of HC03- in intestinal fluid
- dehydration ->poor perfusion->increased lactate-> metabolic acidosis
- main goals:
- manage the underlying disease
- restore renal perfusion
- treatment with HC03- often causes more complications
What is the effect of vomiting on acid-base?
What are the main goals of treatment?
- loss of Cl- ->metabolic alkalosis
- renal compensatory excretion of HC03- is efficient if renal perfusion is adequate
- may combine with lactic acidosis
- main goals:
- manage the underlying disease
- restore renal perfusion
