Intestines Flashcards

1
Q

Where does the final breakdown of disaccharides into monosaccharides occur?

A

brush boarder of duodenum and ileum

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2
Q

What bond does amylase break?

A

1-4 glycosidic bonds (straight) in starch and glycogen

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3
Q

What breaks the 1-6 glycosidic bonds which make branched chains?

A

Isomaltase

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4
Q

What does alpha dextrins do?

A

break multiple close by 1-4 glycosidic bonds to create smaller clumps of amylopectin (short, branched glucose clumps)

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5
Q

How is fructose absorbed?

A

through GLUT5 transporters down diffusion graidents

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6
Q

How do oral rehydration tablets work?

A

Contains glucose, salt and water. Glucose stimulates increased Na+ reabsobtion via Na- Glucose co transport. More Na moving in= more water moving in with it.

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7
Q

What activates pancreatic zymogens?

A

trypsin (this itself is activated in the duodenum lumen by enteropeptidase)

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8
Q

What is the difference between enteropeptidases and exopeptidases?

A

Enteropeptidases= break peptide bonds in middle of chain (elastase, trypsin ect) Exopeptidases= break bonds at end of chains (carboxypeptidase A and B)

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9
Q

How are amino acids/ di and tripeptides absorbed in the intestine?

A

amino acids co transported w/ sodium,di and tripeptides H+ co transport by peptide transporter 1 (and then cytosolic peptidases convert them into amino acids

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10
Q

What is the difference between water absorbtion in the small intestine and the large intestine

A

Small= passive- moves with electrolytes Large= specific aldosterone induced Na+ channels (active)

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11
Q

Describe the process of calcium absorbtion in the intestine when calcium stores are low/ PTH is high.

A
  • Facilitated diffusion on apical side - It binds to calbidin so it can diffuse through the cell - PMCA removes it on basal side - Process requires Vit D for calbidin and PTH to stimulate it -When Ca2+ is normal/ high it just absorbes by passive, paracellular diffusion
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12
Q

How is iron absorbed in the intestines?

A

Needs to be oxidised to Fe2+ (generally by HCl in stomach). The binds to DMT and enters the enterocyte If iron deficient it will bind to the transferrin channel on the basal membrane and be transported to areas in need (induced by low hepcidin) If high iron, it is complexed to ferritin and trapped in the enterocytes. It is lost when the enterocyte is replaced.

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13
Q

Why can proton pump inhibitors lead to iron deficiency?

A

Stomach acid is needed to oxidise Fe3+ to Fe2+

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14
Q

How are most vitamins absorbed?

A

Na+ cotransport

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15
Q

Where are B12+ IF complexes absorbed?

A

terminal ileum

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16
Q

What are coeliacs intolerant to?

A

Gliadin (part of gluten). This is found in wheat, rye and barley.

17
Q

What is the pathophysiology of coeliac disease?

A

An immune response is triggered, which leads to mucosa damage; loss of villi, lengthening of crypts and lymphocytes infiltrating the epithelium.

18
Q

Why do coeliacs get loos stools, bloating and flatulence?

A

Loose stools because less sugar is absorbed, meaning more osmotic stuff is left in the colon lumen so less water absorbed and more water is in the stool. This sugar is fermented by bacteria in the colon, converting it into gas, which causes the bloating and flatulence.

19
Q

What investigations would be done on someone with coeliac disease?

A

Upper GI endoscopy, colonoscopy, serology, anaemia, electrolyte imbalences

20
Q

Describe 2 macroscopic differences between large and small bowel?

A
  • Large intestine has no villi, only crypts - Large intestine has no plicae circularis, but it does have sacculations called haustra
21
Q

Describe the musculature of the large intestine

A
  • 3 londitudional bands (collectively called teniae coli) - intermittant circular bands come off of the teniae coli, contractions of these form the haustra
22
Q

How is water absorbed in the colon and where does it predominate?

A

By ENaC, induced by aldosterone. Mostly in the ascending and traversing colon

23
Q

Which areas are affected by crohns and UC?

A

Crohns: anywhere in GI tract but mainly terminal ileum UC: tends to start in rectum and spreads upwards, almost exclusively affects large bowel

24
Q

What is the difference in depth of legions between UC and Crohns?

A

In crohns the legions are deep and go through all the wall. In UC it tends to be superficial inflammation

25
Q

Which, of crohns and UC, has skip legions, and which has a continuous distribution?

A

Crohns has skip legions, UC is continious

26
Q

Describe some extra intestinal manifestations of inflammatory bowel disease

A

50% have arthiritis/ MSK problems 30% have skin problems (psoriasis, erythema nodosum) Some have liver and billary tree problems 5% get eye problems

27
Q

List factors implicated in triggering inflammatory bowel disease

A

Smoking Antibiotics infections Diet

28
Q

Describe the common presentation of crohns (Age, presenting complaint, bloody/ non bloody stool, any pain/ fever/ anaemia?

A

Young- peak incidence 15-30 and again at 60 PC= many (>4) loose, non bloody stools, weight loss RLQ pain Low grade fever MIild anaemia

29
Q

Would perianal disease be seen in crohns, UC or both?

A

very rare in UC, usually crohns

30
Q

Describe the gross pathological features of crohns (eg seen on colonoscopy)

A
  • Bowel looks red, raw an inflamed - Mucosal odema - Cobblestone appearance - Superfical and deep ulcers - Narrowing of lumen/ wall thickening - Fistulas
31
Q

What microscopic finding is characteristic of crohns?

A

Granulomas

32
Q

Describe the common presentation of UC (Age, presenting complaint, bloody/ non bloody stool, any pain/ fever/ anaemia?

A

Generally affects young adults PC= >4 loose, often bloody stools p/d Weight loss Mild lower abdo pain and cramping No fever

33
Q

What microscopic finding is quite characteristic of UC?

A

crypt abcesses

34
Q

What is the name for this finding following a barium enema? What IBD does it indicate?

A

Lead pipe colon

Found in chronic UC

35
Q

Other than lead pipe colon, state 4 gross pathological changes seen in UC?

A
  • Chronic inflammation of lamina propria
  • Crypt abcesses/ ulcers/ distrosion
  • Pseudopolyps
  • loss of haustra
  • Flat, red and blood appearance to epithelium
  • Dilation of lumen/ narrowing of wall
36
Q

How can inflammatory bowel diseases be treated?

A

Aminosalicylates (for flares and maintain remission)

Corticosteroids (for flares only)

Immunomodulators (for fistulas and maintain remission, only used when first two dont work)

Surgery

37
Q

Describe the surgical options for crohns and UC and when theyre implicated

A

For UC- colectomy will cure but only done when inflammation not settling and start to see precancerous changes.

For crohns- you can remove small bits of affected bowel but this is not usually done because it just appears somewhere else