Describe the features of the jejunum and the ileum.
• Jejunum – thick intestinal wall, red in colour, longer vasa recta
• Ileum – Thin intestinal wall, pink in colour, shorter vasa recta.
What are the 4 parts of the large intestine?
1. Cecum and appendix
2. Colon (ascending, transverse, descending, sigmoid)
4. Anal canal
Describe the histological features of the Large Intestine.
• Thick mucosa with deep crypts and no villi, unlike small intestine.
• Columnar absorptive cells with many goblet cells.
Describe the histological features of the small intestine. Describe how cell renewal occurs in the small intestine. How does the small intestine absorb nutrients?
Mucosa of small intestine is folded into villi:
• Villi separated by crypts
• Cells multiply in crypts and migrate towards tips of villi maturing as they go, acquiring the capacity to absorb.
• They are then shed form the villus tips and mucosa is constantly renewed.
Cells on villi secrete enzymes into brush border which forms an unstirred layer:
o Almost digested nutrients diffuse into this layer and trapped enzymes complete digestion
o Steady release of small molecules for absorption
what type of bonds do salvial and duodenal amylases break? What bond remains?
alpha 1,4 bonds broken
alpha 1,6 bonds remain
How are the alpha 1,6 bonds broken down? What enzymes are used and from where are they secreted?
isomaltase cleaves alpha 1,6 bonds
maltase, sucrase and lactase break down the remaining sugars.
Secreted into brush border from epithelial cells
Describe how glucose is absorbed into the intestinal epithelial cells. What is the name of the receptor that takes glucose into the cell? What is the name of the receptor that takes glucose into the blood stream?
1) Sodium conc gradient generated by na-k-atpase on the basolateral side.
2) SGLT1 on luminal side absorbs sodium and glucose
3) GLUT2 on basolateral membrane absorbs glucose into bloodstream
Using your knowledge of how glucose is absorbed in the intestines, explain what oral rehydration fluid needs to contain and why.
Should contain glucose and salt.
Na and glucose co transported into intestinal epithelial cell.
What enzymes are used to break down peptides? How does each peptidase function?
o Trypsin – Cleaves bonds near Basic AAs
o Chymotrypsin – Cleaves bonds near aromatic AAs
o Carboxypeptidase – Cleaves C terminal AAs with basic side chains
How are amino acids absorbed in the brush border?
• There are at least 5 Na+/AA co-transporters
• Uptake is like that of glucose where the AAs are cotransported down the sodium conc gradient.
• Di and tripeptides taken up by antiporter with H+
How is sodium, chloride and water absorbed in the intestines?
• Sodium taken in via diffusion and active transport
• Chloride follows
• Osmotic gradient from absorption leads to uptake of water
How is calcium absorbed in the intestines? What cofactors are needed? What stimulates its absorption?
• Enters via facilitated diffusion due to low intracellular conc (10-5 moles)
• Pumped out of basolateral membrane via Ca-ATPase – Cofactor Vit D needed. PTH stimulates more calcium absorption and more calcium secretion from bones
What needs to be done to iron to absorb it? How is this achieved? How is iron absorbed.
• Iron is bound to molecules and therefore needs to be solubilised.
• Gastric acid solubilises the Fe into iron complexes
• Gastroferrin (secreted from stomach) then latches onto the iron and prevents it being resequestered.
• Mucosal cells secrete transferrin. Complex is taken into the cells via RME (receptor mediated endocytosis). Once inside Fe is liberated and exported to blood where it binds to transferrin again
How are water soluble vitamins absorbed? How is vitamin b12 absorbed?
• Water soluble vitamins absorbed via passive diffusion (vit C, B vitamins)
• Vit b12 absorbed with co-factor in terminal ileum only:
o Cofactor is intrinsic factor secreted by stomach mucosa
What happens in B12 deficiency? How can it occur?
Pernicious anaemia, B12 critical for production of RBCs.
Can occur due to stomach damage or removal of terminal ileum
Describe the process of segmenting in the small intestines.
1) pacemakers located at frequent intervals down the small intestine. They fire at different rates - highest at stomach end and lowest at large intestine end, "intestinal gradient"
2) Pacemaker fires, but contraction of muscles only occurs at intervals
3) Creates compartments of squeezing and agitation, allowing presentation of new material to mucosa
4) Intestinal gradient used to propel material down the gut.
What is haustral shuttling?
Large intestine equivalent of segmentation
What is mass movement? How often does it occur? How is it triggered?
• Once or twice a day
• Peristaltic pattern from transverse through descending colon, forcing faeces into rectum and induces urge to defecate (triggered by eating via the gastro-colic reflex)
What gives the urge to defecate?
pressure receptors and waves of contraction in the rectal muscle
What are the 2 types of anal sphincters? What type of muscle are they?
o Internal – smooth muscle controlled by PS control
o External – striated muscle
What is the prevailing theory behind why CD and UC occur?
• Immune dysfunction that causes inappropriate immune activation in response to luminal MOs.
• It is thought that alterations to gut flora result in CD or UC.
How would you determine a diagnosis of inflammatory bowel diseae?
Give the predominating features of CD that are not found in UC.
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4) submucosal inflammation
Give the predominating features of UC that are not found in CD.
Continuous rectal involvement results in gross bleeding and mucosal friability
1) Only in colon,
2) continuous anatomical distribution
3) Rectal involvement
4) Mucosal friability (crumbling)
5) Gross bleeding
Why is it difficult to differentiate diagnostically between UC and CD? What are the clinical symptoms of both?
Similar clinical symptoms:
• Abdominal pain, cramping or swelling
• Gastrointestinal bleeding
• Joint pain
• Persistent or recurrent diarrhea
• Weight loss
How do you manage CD?
First get the disease into remission and then maintain remission
Remission achieved by:
o Aminosalicylate anti inflammatory drugs – mild to moderate CD
o Corticosteroid anti inflammatory drugs – moderate to severe CD
Maintenance achieved using immunosuppressing drugs.
How do you manage UC?
First get disease into remission and then maintain remission
Remission achieved by:
o Aminosalicylate anti inflammatory drugs
o Can use corticosteroids in conjunction with aminosalicylate anti inflammatory drugs
Maintenance achieved using immunosuppressing drugs
Can be cured by surgically removing diseased portions of intestine. Necessary in cases with carcinoma of the bowel or severe colitis