Week 8 Flashcards

1
Q

Properties of chyme leaving the duodenum

A

Isotonic
Neutral
Partly digested

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2
Q

Functions and adaptations of the Jejunum and ileum

A

Digestion
Absorbs nutrients, electrolytes and water

Villi, microvilli and plicae circulares increase surface area
Plicae circulares also slow transit time

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3
Q

What are contained in intestinal crypts

A
Enterocytes
Enteroendocrine cells
Goblet cells
Stem cells
Paneth cells
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4
Q

What carbohydrates can be absorbed in the small intestine

A

Monosaccharides only:
Glucose
Fructose
Galactose

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5
Q

Common dietary carbohydrates

A

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

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6
Q

Describe starch

A

20% amylose - has alpha 1,4 glycosidic bonds

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

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7
Q

Describe starch digestion

A

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)

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8
Q

How are monosaccharides absorbed

A

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

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9
Q

How does oral rehydration therapy work

A

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

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10
Q

What proteins can be absorbed in the small intestine

A

Amino acids
Dipeptides
Tripeptides

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11
Q

How does protein absorption differ in babies

A

Can absorb immunoglobulins from breast milk

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12
Q

What activates trypsinogen

A

Enters peptides on the brush border

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13
Q

What are exopeptidases and give examples

A

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

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14
Q

What are endopeptidases and give examples

A

Break peptide bonds in the middle of the polypeptide to produce shorter polypeptides
E.g trypsin, chymotrypsin and elastase

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15
Q

How are amino acids absorbed in the small intestine

A

Enter enterocytes via Na-AA cotransporters

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16
Q

How are dipeptides and tripeptides absorbed in the small intestine

A

Enter enterocytes via H+ transporters such as peptide transporter 1 (PepT1)
Cytosolic peptidases convert them to amino acids

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17
Q

Describe Ca uptake when there is low Ca intake

A

Enter enterocytes via Ca channels
Cross basolateral membrane via Ca2+-ATPase which requires calcitriol (activates calbindin which shuttles calcium to the basolateral membrane)

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18
Q

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

A

Passive paracellular absorption

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19
Q

How does iron enter enterocytes and what is the stomachs role

A

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

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20
Q

What happens to absorbed iron if iron levels are low

A

Binds to transferrin (secreted by intestinal mucosa) and is transported to stores such as spleen, liver, bone marrow and Hb

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21
Q

What happens to absorbed iron if iron levels are high

A

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

22
Q

How are water soluble vitamins absorbed in the small intestine

A

Na cotransport

23
Q

What vitamins does the large intestine absorb

A

Vitamins synthesised by colonic bacteria

24
Q

How is vitamin B12 absorbed

A

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