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Semester 3 - Gastrointestinal > 10. The Intestines > Flashcards

10. The Intestines Flashcards

1
Q

What size of carbohydrates can be absorbed and what are the main ones that are absorbed?

A

Only monosaccharides (glucose, fructose, galactose)

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2
Q

What happens to carbohydrates of plant origin that cannot be digested in SI?

A

• These are utilised and partially digested by bacteria in the colon (providing nutrients for colonic mucosa)

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3
Q

Which ion does glucose enter with?

A

Na+

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4
Q

Give 3 examples of common dietary carbohydrates

A

Starch, lactose and sucrose

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5
Q

What chains does starch consist of and what bonds are present?

A
  • Straight chains of glucose- Amylose (alpha 1-4)

* Branched chains of glucose-Amylopectin (alpha 1-6)

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6
Q

Which enzymes are required to break the bonds in amylose and amylopectin?

A

Amylose (alpha 1-4): salivary and pancreatic amylase

Amylopectin (alpha 1-6): isomaltase (brush border)

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7
Q

What is produced from amylopectin when the alpha 1-4 bonds are broken?

A

alpha Dextrin (shorter but still branched chains of glucose)

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8
Q

What are the products from digestion of starch?

A
  • Glucose (fine)
  • Maltose (maltase) = Glucose + Glucose
  • Alpha dextrins (isomaltase) = Glucose
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9
Q

Which enzymes digests the disaccharides?

A

Lactose (lactase) = glucose + galactose
Sucrose (sucrase) = glucose + fructose
maltose (maltase) = glucose + glucose
(brush border enzymes)

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10
Q

What maintains the Na+ ions concentration gradient in the enterocytes?

A

Na+/K+ ATPase (3Na+ out, 2K+ in) on basolateral membrane

• Maintains low intracellular Na+

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11
Q

How do glucose enter enterocytes?

A

SGLT -1 binds Na+
• This allows glucose binding
• Na+ & glucose moves into cell

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12
Q

How does glucose get from the enterocytes into the blood?

A

GLUT2 transports glucose out of enterocyte

• Diffuses down gradient into capillary blood

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13
Q

How does fructose enter enterocytes?

A

Fructose uses GLUT5 transporter to enter enterocyte

• Facilitated diffusion

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14
Q

Which 4 places do proteins get digested and by what?

A
  1. Stomach- (H+/pepsin)
  2. Intestinal lumen- (Trypsin…)
  3. Brush border
  4. Cytosol (cytosolic peptidases)
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15
Q

Where is pepsinogen released from and what causes its activation?

A

Chief cells in the stomach, converted to pepsin by HCL

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16
Q

What are the products of protein digestion by pepsin?

A
  • Oligopeptides/amino acids

* Move to small intestine

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17
Q

In what form does the pancreas release proteases?

A

Pancreas releases proteases as zymogens –(move into intestinal lumen to be activated)
• Trypsinogen is important

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18
Q

What activates trypsinogen?

A

Enteropeptidase (enterokinase)

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19
Q

What does trypsin lead to activation of?

A

Various other proenzymes:

  • Trypsinogen
  • chymotrypsinogen
  • proelastase
  • procarboxypeptidase A
  • procarboxypeptidase B
20
Q

What is the difference between endo and exopeptidase?

A

Endo: breaks bonds in the middle of the polypeptide to produce shorter polypeptides
Exo: Breaks bonds at the end of polypeptides to produce dipeptides and amino acids

21
Q

Give examples of endo and exopeptidases.

A

Endo: trypsin, chymotrypsin, elastase
Exo: carboxypeptidase A&B

22
Q

What does the brush border contain that aids protein digestion?

A

Brush border- also contains proteases
•The enterocytes express peptidases in their brush border
•Sometimes cannot completely digest proteins down to amino acids

23
Q

What size peptides can be absorbed?

A

short peptides and amino acidds

24
Q

Which transporter absorbs di/tripeptides?

A

PepT1 (peptide transporter 1)

25
Q

How are amino acids transported into enterocytes?

A

• Na+-amino acid co-transporters

26
Q

What happens to the small peptides in enterocytes?

A
  • The small peptides are then acted on by cytosolic peptidases (broken down to amino acids)
  • Certain di- and tri-peptides can also be absorbed into blood
27
Q

How is water absorbed?

A

Absorption driven by movement of sodium into enterocytes
•Na+ moved by active transport out of cell on basolateral membrane
• Na+ diffuses into epithelial cells
• Water then moves by osmosis
• Movement occurs through para-cellular and transcellular paths
*Osmotic gradient from all absorption leads to uptake of water
◦ Fluid absorbed is isosmotic

28
Q

What is the difference in Sodium uptake between small and large intestine?

A

• Both have Na+-k+ ATPase on basolateral membrane
• Apical membrane
- Small intestine- Na+ is co-transported with (glucose, amino acids…)
- Large intestine- Na+ channels

29
Q

What hormone induces Na+ channels in the large intestine?

A

Aldosterone, increases Na+ uptake when blood pressure is low

30
Q

What is the principle of oral rehydration therapy?

A

Mixture of glucose and salt will stimulate maximum water uptake:

  • glucose stimulates Na+ uptake
  • Na+ uptake creates osmotic gradient so water follows
31
Q

What is secretion of water driven by?

A

Chloride movement (predominantly)

32
Q

Describe the mechanism for Chloride ion secretion.

A
  • Chloride enters crypt epithelial cell, Co-transported with Na and K
  • Cyclic AMP levels increase inside cells
  • Increased cAMP activate CFTR
  • Cl ions are secreted
  • Na is drawn into lumen across tight junctions
  • NaCl secretion creates osmotic gradient
  • Water moves into lumen
33
Q

What does B12 deficiency cause?

A

Megaloblastic anaemia and neurological symptoms

34
Q

What are the causes of B12 deficiency?

A

•Lack of intrinsic factor (IF is released by parietal cells)
- B12 is bound to IF in the small intestine and transports this to distal ileum
- Most reabsorbed
•Hypochlorhydria (inadequate stomach acid)
- Acid is important in initially releasing cobalamin
- Gastric atrophy, PPIs
•Inadequate intake in food (strict vegetarians)
•Inflammatory disorders of ileum (where it is absorbed)
- Crohn’s disease

35
Q

What is lactose intolerance?

A

Caused by deficiency of the enzyme lactase (brush border enzyme)
•After the age of 2 years the enzyme is expressed less

36
Q

Why do symptoms of lactose intolerance occur?

A

When lactose is consumed in quantity it cannot be absorbed
• Remains in gut lumen created high osmotic effect
• Water is not absorbed resulting in diarrhoea
• Lactose is fermented in gut producing flatus/bloating

37
Q

What are the symptoms of irritable bowel syndrome?

A
  • Abdominal pain (often cramping, sometimes relieved by defaecation)
  • Bloating
  • Flatulence
  • Diarrhoea/constipation (sometimes alternating)
  • Rectal urgency
38
Q

Who are IBS more common in?

A
  • More common in females vs males (2:1)
  • 20s-40s most affected age range
  • More common in association with psychological disorders
39
Q

What is the cause of IBS?

A

Causes are multifactoria

40
Q

What is coeliac disease?

A

Immunological response to the gliadin fraction of gluten (found in wheat, rye, barley)

41
Q

What damage does coeliac disease cause?

A

Damages mucosa of intestines
• Absence of intestinal villi
• Hypertrophy/Lengthening of intestinal crypts
• Lymphocytes infiltrate epithelium and lamina propria
• Impaired digestion/malabsorption

42
Q

What are the symptoms of coeliac disease?

A
  • Majority related to malabsorption (diarrhoea, weight loss, flatulence, abdo pain)
  • Anaemia (impaired iron absorption), neurological symptoms (hypocalcaemia)
43
Q

How do genetic factors affect coeliac disease?

A 
Genetic factors (high concordance monozygotic twins (75%)
• Very common (underdiagnosed) estimates of 1% of western population affected
44
Q

What are the investigations for coeliac disease?

A

• Bloods- Immunoglobulin A (IgA) antibodies to smooth muscle endomysium and tissue
transglutaminase
• Upper GI endoscopy + biopsies (duodenum)
• Mucosal pathology
• Villi are reduced or absent

45
Q

What is the treatment for coeliac disease?

A
  • Diet- strict gluten free diet
  • Clinical improvement quite quick (days/ weeks)
  • Histological improvement (weeks/months

Semester 3 - Gastrointestinal (17 decks)

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