The Intestines Flashcards
Main differences between jejunum and ileum
Jejunum: Upper left quadrant Thick wall Longer vasa recta (straight arteries) Less arcades (arterial loops)
Ileum: Lower right quadrant Thin wall Shorter vasa recta More arcades
What supplies Blood to the colon?
Caecum - ileocolic artery (SMA)
Ascending colon- right colic artery (SMA)
Transverse colon - middle colic artery (branch of superior mesenteric a)
Descending colon - left colic artery (IMA)
What supplies blood to the small intestine?
Jejunum and ileal arteries
(Anastomoses of SMA)
Duodenum proximal- gastroduodenal a and superior pancreaticoduodenal a
Distal- SMA and inferior pancreaticoduodenal a
Venous drainage of the intestines?
Veins -> superior mesenteric vein -> portal vein (-> behind neck of pancreas-> liver)
- portal vein, splenic vein, SMV, Srectal vein -> IMV all join within liver
What do all the terminal branches of the superior mesenteric artery anastomoses to become?
Marginal artery (right and left)
What 2 factors are important for absorption in the gut?
Large surface area - mucosa folded into villi, enterocytes covered in micro villi (brush border). Permanent folds in mucosal membrane SI - pilcae circulares
Slow movements of contents in peristalsis - precise control required. Segmentation - contraction distal and proximal (back and forth in gut)
Epithelial cells of the intestine
Enterocytes (most of cells) - absorptive cells, tall, columnar
Goblet cells -> mucus
Enteroendercrine cells -> peptide hormones
What are the crypts of Lieberkuhn? What cells are they made up of?
Intestinal gland
Stem cells at base - migrate to surface, maturing as they migrate into various cell types -> transit amplifying cells, goblet cells, enteroendocrine cells, enterocytes
Paneth cells at base (innate mucosal defence cells) - produce antmicrobial peptides
Mucosa is constantly shed 3-6 days
Carbohydrates of plant origin can’t be digested in small intestine so what are they used for?
Dietary fibre - binds bile salts (uses cholesterol so lowers serum cholesterol) and provides nutrients for bacteria in the colon
What does starch consist of?
Straight chain of glucose (amylose polysaccharide)
Alpha 1-4
and branched glucose chains (amylopectin) alpha 1-4 + alpha 1-6
How is starch broken down?
Amylase breaks straight glucose chains into maltose (disaccharide)
And branches chains into alpha-dextrins (disaccharide) alpha 1-4
The chain alpha 1-6 bonds are broken by isomaltase -> maltose
-Maltase breaks down maltose -> glucose
What is lactose made from, what happens if you are lactose intolerant?
Glucose + galactose
If lack lactase can’t break down lactose -> moves into colon & is used by bacteria which produce H2 (fermented-> flatulence) or lactose acts as an osmotic molecule and draws water in -> diarrhoea
After the age of 2 enzyme expressed less
What’s sucrose made from, what breaks it down?
Glucose + fructose
Sucrase
How are monosaccharides absorbed?
Mostly in duodenum and jejunum enterocytes
Basolateral membrane:
-Na+/K+ ATPase maintains low intracellular [Na]
Brush border/ apical:
- SGLT-1 binds Na+ with glucose/ galactose into cell
Basolateral:
-GLUT2 glucose/ galactose/ fructose out into capillary
(Fructose uses GlUT5 to enter celll facilitated transport and can leave by 2 channels)
Locations in order for protein digestion
Stomach (pepsin) -> intestinal lumen (trypsin main) -> brush border of enterocytes -> cytosol of enterocyte (cytosolic peptidases)
What protein digestion occurs in the stomach?
Chief cells -> pepsinogen -> pepsin (by HcL) -> turns proteins into oligopeptides/ AAs -> small intestine
What does the pancreas release that’s important for protein digestion?
Pancreas releases proteases as zymogens (activated in intestinal lumen) e.g. trypsinogen (converted to trypsin by enteropeptidase), trypsin activates: (chymotrypsinogen-> chymotrypsin, proelastase-> elastase, procarboxypeptidase A and B)
What are endopeltidases and exopeptidases, give some examples?
Endopeptidases produce shorter polypeptides by breaking bonds in the middle of polypeptide e.g. trypsin, chymotrypsin, elastase
Exopeptidases produce dipeptides or AAs by breaking bonds at ends of polypeptides e.g. carboxypeptidase A and B
What occurs at the brush border Of enterocytes for protein digestion?
Contains proteases
Intestine can absorb short peptides by peptide transporter 1 (PepT1) co-transporter with H+
Amino acids can be co-transported into cell and then into blood with Na+
What digestion occurs at cytosol of enterocytes?
Small peptides acted on by cytosolic peptidases -> AAs
Certain di/ trip peptidases can be absorbed into blood
How is water absorbed in the intestines?
Driven by movement of sodium into enterocytes
NA/ K ATPase moves sodium out basolateral
- Na diffuses in apical (H+ antiport/ glucose/ AAs co-transporter) small intestine
- Na channels large intestine (ENaC) induced by aldosterone
Isoosmotic Water follows either transcellularly diffuses or paracellularly (through tight junctions) from osmotic gradient
Malabsorption-> diarrhoea
Why is oral rehydration fluid a mixture of water, glucose and salt rather than just water?
Maximum water uptake
Na+ uptake generates osmotic gradient
Glucose uptake stimulates Na uptake
How is water secreted in the intestinal lumen?
Driven predominately by chloride movement
Chloride enters crypts of epithelial cell co-transported with Na and K (NaK2CL) -> increase cAMP levels -> activates CFTR (cystic fibrosis transmembrane conductance regulator) which secretes chloride into lumen (infection can also activate)
Na can be drawn into lumen across tight junctions
NaCl secretion creates osmotic gradient so water moves into lumen
What are some causes of B12 deficiency? What are the consequences?
Lack of intrinsic factor -> pernicious anaemia (B12 binds to in small intestine and then transported to distal ileum)
Hypochlorhydria (inadequate stomach acid) acid initially helps release cobalamin(B12)
Inadequate food intake (veggies)
Inflammatory disorders of ileum e.g. chrohn’s
-megoblastic anaemia, neurological symptoms
What are the symptoms of irritable bowel syndrome, how common is it, risk factors?
Abdo pain, bloating, flatulence, diarrhoea, constipation, rectal urgency
Affects 10-15% adults
More common females (2:1) 20s-40s, more common in association with psychological disorder (poss serotonin lack)
In Absence of documented abnormalities
What is coeliac disease. What foods should be avoided? What are the consequences and symptoms?
Immunological response to gliadin fraction of gluten (wheat, rye, barley)
Fermented sugars in intestine-> damages mucosa of intestines -> absence of intestinal villi, hypertrophy/ lengthening of crypts, lymphocytes infiltrate epithelium and lamina propria, impaired digestion/ malabsorption
Genetic factors
Diarrhoea, weight loss, flatulence, abdo pain, anaemia, neurological symptoms
How to investigate and treat coeliac disease
Bloods: immunoglobulin A (IgA) antibodies to smooth muscle endomysium and tissue transglutaminase
Upper Gi endoscopy and biopsies (duodenum) - mucosal pathology like presence of immune cells, villi reduced/ absent
✅ strict gluten free diet (can affect growth of children), clinical improvement days/ weeks, histological weeks/ months
