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Flashcards in Week 8 Deck (51):
1

Properties of chyme leaving the duodenum

Isotonic
Neutral
Partly digested

2

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

3

What are contained in intestinal crypts

Enterocytes
Enteroendocrine cells
Goblet cells
Stem cells
Paneth cells

4

What carbohydrates can be absorbed in the small intestine

Monosaccharides only:
Glucose
Fructose
Galactose

5

Common dietary carbohydrates

Starch (glucose polysaccharide)
Sucrose (glucose-fructose)
Lactose (glucose-galactose)

6

Describe starch

20% amylose - has alpha 1,4 glycosidic bonds
80% amylopectin - has alpha 1,4 and 1,6 glycosidic bonds

7

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)

8

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

9

How does oral rehydration therapy work

Mixture of
Water
Glucose - to stimulate Na uptake
Na - to stimulate water uptake

10

What proteins can be absorbed in the small intestine

Amino acids
Dipeptides
Tripeptides

11

How does protein absorption differ in babies

Can absorb immunoglobulins from breast milk

12

What activates trypsinogen

Enters peptides on the brush border

13

What are exopeptidases and give examples

Break peptide bonds at the ends of the polypeptide to produce amino acids or dipeptides
E.g carboxypeptidase

14

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

15

How are amino acids absorbed in the small intestine

Enter enterocytes via Na-AA cotransporters

16

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

17

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)

18

Describe calcium uptake when there is a high or normal calcium intake

Passive paracellular absorption

19

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

20

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

21

What happens to absorbed iron if iron levels are high

Contained in ferritin complexes so it is lost when the enterocyte dies

22

How are water soluble vitamins absorbed in the small intestine

Na cotransport

23

What vitamins does the large intestine absorb

Vitamins synthesised by colonic bacteria

24

How is vitamin B12 absorbed

Bound to intrinsic factor (secreted by parietal cells) to make it soluble
In the terminal ileum

25

Causes of B12 deficiency

Autoimmune destruction of parietal cells (also causes chronic gastritis)
Terminal ileum removal e.g Chron's disease

26

Describe motility of the small intestine

1. Intestinal gradient BETWEEN meals - pacemakers have a higher frequency proximally which drives distal progression of contents
2. Segmentation FOLLOWING meals - contents move back and forth to control transit
3. Peristalsis

27

Describe motility of the large intestine

1. Haustral shuttling - segmentation in proximal colon allows remaining water to be absorbed
2. Mass movement (gastrocolic reflex) - contents move rapidly from transverse colon to rectum following meals

28

What stretch level in the rectum gives urge to defaecate

25%

29

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

30

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

31

What is IBD

Inflammatory bowel disease - idiopathic inflammation of GI tract

32

Causes of IBD

Genetic
Environment - NSAIDs, early appendectomy, colonic bacteria, smoking (Chron's only)
Triggers - antibiotics, acute infections, smoking, diet, NSAIDs

33

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

34

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

35

Typical presentation of UC

Rectal bleeding
Diarrhoea
Abdominal pain
Extra intestinal symptoms

36

What is lead pipe colon

Featureless colon die to loss of haustra in distal colon

37

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

38

Compare demographics of Chron's and UC

Chron's - peaks at 15-30 and 60+
UC - Young adults, usually female

39

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

40

Compare depth of inflammation of Chron's and UC

Chron's - transmural
UC - mucosal

41

Compare pattern of inflammation of Chron's and UC

Chron's - skip lesions
UC - continuous

42

Compare macroscopic appearance of Chron's and UC

Chron's - cobblestone
UC - pseudopolyps

43

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)

44

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

45

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

46

Investigations for UC

Colonoscopy - biopsy
Abdominal X-ray - exclude colonic dilation
Bloods - anaemia and serum markers
Stool culture - rectal bleeding

47

Diagnosis if investigations cant distinguish between Chron's and UC

Indeterminate colitis

48

Pharmacological treatment of IBD

Aminosalicylates e.g sulfasalazine - flares and remission
Corticosteroids e.g prednisolone - flares
Immunomodulators - maintain remission

49

Examples of immunomodulators and how they work

Azathioprine
Infliximab - induce TNF alpha bound cells to undergo apoptosis

50

Surgery options for Chron's

Not curative:
Resolve complications such as strictures or fistulae
Colectomy (remove as little as possible)

51

Surgery options for UC

Curative:
Subtotal colectomy