8. The Intestines Flashcards Preview

13. Gastrointestinal > 8. The Intestines > Flashcards

Flashcards in 8. The Intestines Deck (94):
1

What happens to the chyme that is emptied into the duodenum?

It is conditions, acidity is correct by HCO3- secretion from pancreas, liver, and duodenal mucosa. Hypertonicity corrected by osmotic movement of water into duodenum across wall. Partly digested nature correct for by complete digestion by enzymes from pancreas and duodenal mucosa, with bile acids from liver.

2

What makes the small intestines good for absorption?

Large surface area that contents is exposed to through gentle agitation for hours.

3

How is the small intestine surface area so big?

Millons of villi project into the lumen.

4

How is the brush border of the small intestines formed?

The epithelial cells arise by rapid division in the crypts between villi and migrate towards the tips to be shed. They mature as they migrate and the luminal surface gets covered with millions of microvilli.

5

What is the purpose of the small intestine brush border?

Increasing the surface layer, it forms an 'unstirred layer' where nutrients meet and react with enzymes secreted by enterocytes, completing digestion prior to absorption.

6

What is the function of the large intestines?

Absorb water from the indigestible residues of chyme and convert them into semi-solid stool or faeces that is stored temporarily.

7

What are teniae coli?

Thickened bands of smooth muscle, running the length of the large intestines.

8

What are haustra?

The shortened part of the walls that are sacculated between the teniae.

9

What are the functions of the whole small intestine?

Secrete protease/ carbohydrase enzymes to complete digestions, secrete hormones - secretin, gastrin, cholecystokinin.

10

What are the functions of the duodenum?

Bile and pancreatic secretions added via ampulla of vater, secrete HCO3- to neutralise chyme, osmotic movement of water in to make chyme more hypotonic, absorption of iron.

11

What are the functions of the jejunum?

Absorption fo carbohydrate and amino acids. Fatty acids, vitamins, mineral, electrolytes, and water soak through vili.

12

What are the functions of the ileum?

Absorption of vitamin B12, bile, and anything not absorbed by the jejunum.

13

How long is food in the large intestine for?

16 hours to finish digestion.

14

What are the functions of the large intestines?

Absorption of water, any remaining absorbable nutrients, vitamins created by colonic bacteria (vitamin K, B12, thiamine, riboflavin). Sends indigestible matter to the rectum.

15

What is the function of the rectum?

To store and compact faecal matter for defaecation.

16

How are a-amylases important in absorption?

They break a1-4 bonds and are secreted in saliva and by the pancreas. They yield glucose and maltose from amyloses and a-limit dextrins from amylopectins.

17

How do brush border enzymes complete breakdown of glucose?

Isomaltase breaks down branched molecules at a1,6 bonds. Maltase breaks maltose to glucose. Sucrase breaks sucrose to glucose and fructose diamer. Lactase breaks lactose to glucose and galactose diamer.

18

How is glucose absorbed in the gut?

Actively using energy from the Na+ gradient from the Na+K+ATPase in the basolateral membrane. Glucose enters the epithelial cell across its apical membrane via Na+/glucose symptorter - SGLT1.

19

How does glucose leave the epithalial cell into the bloodstream across the basolateral membrane?

Via facilitated diffusion through GLUT2 transporter.

20

How does fructose enter cells from the lumen?

Via facilitated diffusion.

21

How are proteins digested to short peptides in the stomach?

By pepsin from chief cells.

22

How are proteins digested to short peptides in the duodenum?

By peptidases from the pancreas.

23

Which bonds do the following enzymes prefer breaking? Pepsin, trypsin, chymotrypsin, carboxypeptidase.

Pepsin - bonds near aromatic AA side chains. Trypsin - bonds near basic AA side chains. Chymotrypsin - bonds near aromatic AA side chains. Carboxypeptidase - C-terminal AA with basic side chains.

24

Why is it useful that neonate guts are open?

They can pick up whole proteins, helpfully including IgA from mother's breast milk for passive immunity.

25

How are amino acids uptaken?

Using Na+/amino acid co-transporters that use the Na+ gradient from the Na+/K+ATPase. Or by facilitated passive diffusion.

26

How are dipeptides and tripeptides taken up?

By active mechanisms associated with pumping H+ into the lumen - then returns by co-transport with the peptide.

27

Why is it hard to digest fats?

Fats are insoluble in water so aggregate into large globules so digestive enzymes can't effectively get at them and the problem is made worse by acid in the stomach.

28

How does the duodenum help with fat digestion?

Bile acids enable fats to be incorporated into small micelles that have a higher surface area for lipases and carry fats to the unstirred layer to slowly diffuse into epithelial cells.

29

What happens to fatty acids when in epithelial cells?

They are reconstituted into triacylglycerols and re-expelled as chylomicrons into the lymphatic system and then systemic veins.

30

How is sodium taken up in the gut?

By diffusion into the cell, then actively transported across basolateral membrane by NaKATPase.

31

How is chloride taken up in the gut?

Following the movements of Na+ across the apical then basolateral membranes.

32

What is the results of uptake of Na+ and Cl-?

An osmotic gradient, so leads to water uptake.

33

What proportion of ingested calcium is absorbed?

About 10%.

34

How is calcium absorbed?

Enters cell by facilitated diffusion due to low intracellular concentration. It is then pumped across basolateral membrane by Ca2+ ATPase.

35

What does calcium absorption require?

Vitamin D.

36

What is calcium absorption stimulated by?

Parathyroid hormone (PTH).

37

What forms of iron can be absorbed?

Ferrous form - Fe2+.

38

How does the gut maximise iron absorption?

Gastric acid solubises iron complexes to make them ferrous, and the stomach also secretes gastroferrin (binds iron and keeps it ferrous).

39

What is the consequence of intestinal mucosal cells secreting transferrin?

Binds to ferrous iron in the lumen. Complex is taken into cells by endocytosis, split and the iron is exported to the blood to bind again to transferring.

40

Which vitamins are absorbed by passive diffusion?

Water-soluble vitamins - C, and B.

41

How is vitamin B12 absorbed?

With a co-factor in the terminal ileum. Intrinsic factor keeps it soluble by binding in the stomach (secreted by stomach mucosa).

42

What is pernicious anaemia a result of?

Vitamin B12 deficiency.

43

When does pernicious anaemia occur?

With damage to the stomach, preventing it from secreting intrinsic factor, or the terminal ileum has been damaged or removed.

44

What is the basis of oral rehydration therapy?

Uptake of Na+ generates an osmotic gradient, which water follows. Glucose uptake stimulates Na+ uptake and generates its own osmotic gradient. So a mixture of NaCl and glucose stimulates maximum water uptake.

45

Why must the intestinal contents move slowly whilst being gently agitated?

For effective absorption.

46

What is the pattern of motility of the small intestine?

Segmenting.

47

How is the intestinal gradient created?

The small intestine is divided into sections, each with a pacemaker. The frequency of the pacemakers get less as you go distal, so contraction slowing down means food is moved caudally.

48

What is the large intestine divided into?

Segments called haustra.

49

How is contents of the large intestine moved back and forth?

By contraction of the smooth muscle in the walls of the Haustra.

50

What is mass movement?

Peristaltic propelling from the transverse through to the descending colon which forces faeces into the rectum, inducing the urge to defecate.

51

What normally triggers mass movement?

Eating, the gastro-colic reflex.

52

What makes up the internal anal sphincter?

Smooth muscle.

53

What controls the internal anal sphincter?

Parasympathetic control to make it relax.

54

What makes up the external anal sphincter?

Voluntary striated muscle.

55

What controls the external anal sphincter?

Voluntary control to relax the muscle.

56

How is faeces expelled?

Relaxation of the internal and external anal sphincters paired with increased intra-abdominal pressure.

57

When is the voluntary control of the external anal sphincter overriden?

When the rectal pressure become too high.

58

What are the causes of intestinal inflammation and infection?

Ulcerative colitis, Crohn's disease, diversion colitis, diverticular colitis, radiation, drug, infectious, ischaemic colic.

59

What is ulcerative colitis?

An inflammatory disorder that affects the rectum and extends proximally in continuity to affect a variable extent of the colon.

60

In which populations is ulcerative colitis more prevalent?

US, UK, northern Europe, young adults, females.

61

What is the mucosa of UC patients dominated by?

Th2 (T-helper) cells, which produce transforming growth factor (TGF) and IL-5.

62

What is the clinical presentations of ulcerative colitis?

Rectal bleeding, diarrhoea, and abdominal pain.

63

What is Crohn's disease?

A conditions of chronic inflammation potentially involving any location of the GI tract from mouth to anus.

64

What are the two peaks of incidence of Crohn's disease?

Ages 15-30 and then again at 60 years.

65

What is the mucosa of Crohn's patients dominated by?

Th1 (T-helper) cells, which produce interferon gamma (IFN-y) and IL-2.

66

What does presentation of Crohn's depend on?

The disease's location.

67

What is the presentation of Crohn's disease in the upper GI tract?

Nausea and vomiting, dyspepsia, small bowel obstruction, anorexia and weight loss, and loose stools.

68

What is the presentation of Crohn's disease in the colon?

Diarrhoea, passage of obvious blood.

69

Why does terminal ileum involvement of Crohn's disease lead to anaemia?

Poor absorption of vitamin B12.

70

What are the genetic predispositions to inflammatory bowel disease?

IBD1, NOD2/CARD15. Having one copy of a risk allele has a 2-4 fold increased risk, two copies confers a 20-40 fold increase risk.

71

What are the environmental factors that can lead to inflammatory bowel disease?

NSAIDS - altered intestinal barrier, early appendectomy - increased UC incidence, smoking - protective in UC, increases risk of Crohn's.

72

What are the triggers of inflammatory bowel disease?

Antibiotics (gets rid of normal flora), diet, acute infections, NSAIDs, smoking, stress.

73

What are the common methods of investigation for inflammatory bowel disease?

Colonoscopy and biopsies, stool analysis, barium radiographs, CT scans, capsule endoscopy, plain X ray.

74

What are the macroscopic changes to the bowel in Crohn's disease?

Involved bowel is thickened and often narrowed. Deep ulcers and fissures in mucosa cause cobblestone appearance. Fistular and abscesses may be seen in penetrating disease.

75

What are the macroscopic changes to the bowel in ulcerative colitis?

Mucosa is reddened and looks inflamed, bleeding easily. In severe disease, there is extensive ulceration with the adjacent mucosa appearing as inflammatory polyps.

76

What are the microscopic changes of Crohn's disease?

Inflammation through all layers of the bowel, increase in chronic inflammatory cells, lymphoid hyperplasia, and granulomas.

77

What are the microscopic changes of ulcerative colitis?

Superficial inflammation, chronic inflammatory cell infiltrate in the lamina propria, crypt abscesses, goblet cell depletion.

78

What is colitis of undetermined type and aetiology (CUTE)?

Where it is unclear if the patient has Crohn's disease or ulcerative colitis.

79

What are the colonoscopy results of Crohn's?

Mild, patchy surface ulceration - Cobblestoning.

80

Why are the upper GI endoscopy of Crohn's needed?

To exclude oesophageal and gastroduodenal disease in patients with relevant symptoms.

81

What small bowel imaging can be done in investigations for Crohn's?

Barium follow through, CT scan with oral contrast, small bowel ultrasound, MRI, asymmetrical alteration in the mucosal pattern with deep ulceration, and areas of narrowing or stricturing, string sign of Kantor.

82

When are capsule endoscopies taken in Crohn's patients?

If they have normal radiological examinations.

83

What is the gold standard investigation for diagnosing UC?

Colonoscopy with biopsy to assess disease activity and extent.

84

What is a diagnostic imaging sign of ulcerative colitis?

Collar button ulcers - ulcer through bowel mucosa to the muscle, then up and down in a T shape.

85

What are the treatment options for Crohn's disease in induction of remission?

Oral or IV glucocorticosteroids, enteral nutrition, anti-TNF antibodies.

86

What are the treatment options for Crohn's disease in maintaining remmission?

Methotrexate, azathioprine, anti-TNF antibodies.

87

What are the treatment options for Crohn's disease in perianal disease?

Ciprofloxacin and metrronidazole, azathioprine, anti-TNF antibodies.

88

What is the basic action of anti-TNF antibodies?

Binds to membrane bounds TNF-a and induces immune cell apoptosis.

89

When is Crohn's surgically managed?

If there is failure of therapy with acute or chronic symptoms.

90

What is the treatment for distal UC disease?

Topical or suppository corticosteroids.

91

What is the treatment for left sided colitis?

Topical corticosteroid enema.

92

What is the treatment for extensive colitis?

Oral corticosteroids and infliximab.

93

When is UC surgically managed?

In patients with complications of corticosteroid dependence.

94

What is the operation of choice for UC?

Subtotal colectomy with end ileostomy and preservation of the rectum.