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GI > Week 8 > Flashcards

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
Q

Causes of B12 deficiency

A

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

26
Q

Describe motility of the small intestine

A
  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
Q

Describe motility of the large intestine

A
  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
Q

What stretch level in the rectum gives urge to defaecate

A

25%

29
Q

Describe defaecation

A 
Parasympathetic stimulation (pelvic) relaxes internal anal sphincter
Somatic stimulation (pudendal) relaxes external anal sphincter 
Intra abdominal pressure increases leading to expulsion of faeces
30
Q

What is tenesmus

A

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
Q

What is IBD

A

Inflammatory bowel disease - idiopathic inflammation of GI tract

32
Q

Causes of IBD

A

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

33
Q

What are some extra intestinal symptoms of IBD

A 
MSK problems e.g arthritis
Erythema nodusum - mostly affects knees and shins 
Psoriasis
Primary sclerosing cholangitis 
Eye problems
34
Q

Typical presentation of Chron’s disease

A

Upper GI - nausea, loose stools, weight loss
Terminal ileum - anaemia, glossitis, anorexia
Colon - diarrhoea and blood in stool
Extra intestinal symptoms

35
Q

Typical presentation of UC

A

Rectal bleeding
Diarrhoea
Abdominal pain
Extra intestinal symptoms

36
Q

What is lead pipe colon

A

Featureless colon die to loss of haustra in distal colon

37
Q

Compare location of Chron’s and UC

A

Chron’s - anywhere form mouth to anus, but less rectal involvement than UC
UC - rectum and extends proximally with no breaks

38
Q

Compare demographics of Chron’s and UC

A

Chron’s - peaks at 15-30 and 60+

UC - Young adults, usually female

39
Q

Compare inflammatory cell involvement of Chron’s and UC

A

Chron’s - TH1 cells produce interferon gamma and IL2

UC - TH2 cells produce transforming growth factor and IL5

40
Q

Compare depth of inflammation of Chron’s and UC

A

Chron’s - transmural

UC - mucosal

41
Q

Compare pattern of inflammation of Chron’s and UC

A

Chron’s - skip lesions

UC - continuous

42
Q

Compare macroscopic appearance of Chron’s and UC

A

Chron’s - cobblestone

UC - pseudopolyps

43
Q

What features are more common in Chron’s

A

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
Q

What features are more common in UC

A

Crypt abscess
Friable mucosa - bleeds on contact
Ulceration (although a common feature in Chron’s)
Depletion of goblet cells

45
Q

Investigation for Chron’s

A

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
Q

Investigations for UC

A

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

47
Q

Diagnosis if investigations cant distinguish between Chron’s and UC

A

Indeterminate colitis

48
Q

Pharmacological treatment of IBD

A

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

49
Q

Examples of immunomodulators and how they work

A

Azathioprine

Infliximab - induce TNF alpha bound cells to undergo apoptosis

50
Q

Surgery options for Chron’s

A

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

51
Q

Surgery options for UC

A

Curative:

Subtotal colectomy

GI (19 decks)

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