Week 8 Flashcards
Properties of chyme leaving the duodenum
Isotonic
Neutral
Partly digested
Functions and adaptations of the Jejunum and ileum
Digestion
Absorbs nutrients, electrolytes and water
Villi, microvilli and plicae circulares increase surface area
Plicae circulares also slow transit time
What are contained in intestinal crypts
Enterocytes Enteroendocrine cells Goblet cells Stem cells Paneth cells
What carbohydrates can be absorbed in the small intestine
Monosaccharides only:
Glucose
Fructose
Galactose
Common dietary carbohydrates
Starch (glucose polysaccharide)
Sucrose (glucose-fructose)
Lactose (glucose-galactose)
Describe starch
20% amylose - has alpha 1,4 glycosidic bonds
80% amylopectin - has alpha 1,4 and 1,6 glycosidic bonds
Describe starch digestion
Amylase breaks alpha 1,4 bonds to form glucose
Isomaltase breaks alpha 1,6 bonds to break down alpha dextrins
Maltase breaks down maltose (glucose-glucose)
How are monosaccharides absorbed
Na-K-ATPase on basolateral membrane maintains Na gradient for Na and glucose/galactose cotransport via SGLUT1 on the apical membrane. Fructose moves through the apical membrane via GLUT5.
All monosaccharides cross the basolateral membrane through GLUT2 into the blood
How does oral rehydration therapy work
Mixture of
Water
Glucose - to stimulate Na uptake
Na - to stimulate water uptake
What proteins can be absorbed in the small intestine
Amino acids
Dipeptides
Tripeptides
How does protein absorption differ in babies
Can absorb immunoglobulins from breast milk
What activates trypsinogen
Enters peptides on the brush border
What are exopeptidases and give examples
Break peptide bonds at the ends of the polypeptide to produce amino acids or dipeptides
E.g carboxypeptidase
What are endopeptidases and give examples
Break peptide bonds in the middle of the polypeptide to produce shorter polypeptides
E.g trypsin, chymotrypsin and elastase
How are amino acids absorbed in the small intestine
Enter enterocytes via Na-AA cotransporters
How are dipeptides and tripeptides absorbed in the small intestine
Enter enterocytes via H+ transporters such as peptide transporter 1 (PepT1)
Cytosolic peptidases convert them to amino acids
Describe Ca uptake when there is low Ca intake
Enter enterocytes via Ca channels
Cross basolateral membrane via Ca2+-ATPase which requires calcitriol (activates calbindin which shuttles calcium to the basolateral membrane)
Describe calcium uptake when there is a high or normal calcium intake
Passive paracellular absorption
How does iron enter enterocytes and what is the stomachs role
Iron crosses apical membrane via H+ cotransporters in its ferrous form
Stomach produces:
Gastric acid - makes iron ferrous
Gastroferrin - binds iron and keeps it in ferrous form
What happens to absorbed iron if iron levels are low
Binds to transferrin (secreted by intestinal mucosa) and is transported to stores such as spleen, liver, bone marrow and Hb
What happens to absorbed iron if iron levels are high
Contained in ferritin complexes so it is lost when the enterocyte dies
How are water soluble vitamins absorbed in the small intestine
Na cotransport
What vitamins does the large intestine absorb
Vitamins synthesised by colonic bacteria
How is vitamin B12 absorbed
Bound to intrinsic factor (secreted by parietal cells) to make it soluble
In the terminal ileum
Causes of B12 deficiency
Autoimmune destruction of parietal cells (also causes chronic gastritis)
Terminal ileum removal e.g Chron’s disease
Describe motility of the small intestine
- Intestinal gradient BETWEEN meals - pacemakers have a higher frequency proximally which drives distal progression of contents
- Segmentation FOLLOWING meals - contents move back and forth to control transit
- Peristalsis
Describe motility of the large intestine
- Haustral shuttling - segmentation in proximal colon allows remaining water to be absorbed
- Mass movement (gastrocolic reflex) - contents move rapidly from transverse colon to rectum following meals
What stretch level in the rectum gives urge to defaecate
25%
Describe defaecation
Parasympathetic stimulation (pelvic) relaxes internal anal sphincter Somatic stimulation (pudendal) relaxes external anal sphincter Intra abdominal pressure increases leading to expulsion of faeces
What is tenesmus
Mass in rectum stretches the rectum and so causes continuous a urge to defaecate but with little or no stool passed I.e feeling of incomplete defaecation
What is IBD
Inflammatory bowel disease - idiopathic inflammation of GI tract
Causes of IBD
Genetic
Environment - NSAIDs, early appendectomy, colonic bacteria, smoking (Chron’s only)
Triggers - antibiotics, acute infections, smoking, diet, NSAIDs
What are some extra intestinal symptoms of IBD
MSK problems e.g arthritis Erythema nodusum - mostly affects knees and shins Psoriasis Primary sclerosing cholangitis Eye problems
Typical presentation of Chron’s disease
Upper GI - nausea, loose stools, weight loss
Terminal ileum - anaemia, glossitis, anorexia
Colon - diarrhoea and blood in stool
Extra intestinal symptoms
Typical presentation of UC
Rectal bleeding
Diarrhoea
Abdominal pain
Extra intestinal symptoms
What is lead pipe colon
Featureless colon die to loss of haustra in distal colon
Compare location of Chron’s and UC
Chron’s - anywhere form mouth to anus, but less rectal involvement than UC
UC - rectum and extends proximally with no breaks
Compare demographics of Chron’s and UC
Chron’s - peaks at 15-30 and 60+
UC - Young adults, usually female
Compare inflammatory cell involvement of Chron’s and UC
Chron’s - TH1 cells produce interferon gamma and IL2
UC - TH2 cells produce transforming growth factor and IL5
Compare depth of inflammation of Chron’s and UC
Chron’s - transmural
UC - mucosal
Compare pattern of inflammation of Chron’s and UC
Chron’s - skip lesions
UC - continuous
Compare macroscopic appearance of Chron’s and UC
Chron’s - cobblestone
UC - pseudopolyps
What features are more common in Chron’s
Fistulae - to bowel, bladder, vagina or skin
Perianal disease
Granulomas
Fibrosis (string sign of Kantor)
Gross bleeding
Ileal involvement (although 15-20% ileitis in UC)
What features are more common in UC
Crypt abscess
Friable mucosa - bleeds on contact
Ulceration (although a common feature in Chron’s)
Depletion of goblet cells
Investigation for Chron’s
Colonoscopy - cobblestone appearance, get biopsy to find granulomas
CT with contrast - string sign of Kantor, obstruction, extra intestinal issues
Barium enema/follow through - detect strictures or fistulae
Bloods - anaemia
Investigations for UC
Colonoscopy - biopsy
Abdominal X-ray - exclude colonic dilation
Bloods - anaemia and serum markers
Stool culture - rectal bleeding
Diagnosis if investigations cant distinguish between Chron’s and UC
Indeterminate colitis
Pharmacological treatment of IBD
Aminosalicylates e.g sulfasalazine - flares and remission
Corticosteroids e.g prednisolone - flares
Immunomodulators - maintain remission
Examples of immunomodulators and how they work
Azathioprine
Infliximab - induce TNF alpha bound cells to undergo apoptosis
Surgery options for Chron’s
Not curative:
Resolve complications such as strictures or fistulae
Colectomy (remove as little as possible)
Surgery options for UC
Curative:
Subtotal colectomy
