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LSS Alimentary System > 5 Small Intestine > Flashcards

5 Small Intestine Flashcards

1
Q

Q: What is the main function of the small intestine?

A

A: absorb nutrients, salt and water

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2
Q

Q: Where does the small intestine originate and end? How is it functionally separated? (2)

A

A: originates immediately after the stomach, and coils around the abdomen (held in place by the mesentery) until it meets the large intestine in the lower right quadrant

functionally separated from these structures by two sphincters; the pyloric sphincter at the proximal end, and the ileocaecal valve at the distal end.

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3
Q

Q: How is the small intestine organised? (3) separate? Include roles and approximate length

A

A: three portions as listed below (with approximate lengths in parentheses), however where one portion starts and another finishes is less clear as they all have the same basic histological structure.

The duodenum: (0.25 m) - key roles in digestion and gut regulation

The jejunum (2.5 m) - key roles for absorption

The ileum (3.75 m) - key roles for absorption

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4
Q

Q: What is specific about the small intestine wall structure? (5)

A

A: three noteworthy features:

  • epithelial layer has finger-like projections called villi
  • The mucosa is arranged in circular folds (like a concertina)
  • It has invaginations called crypts of Lieberkühn
  • external wall has longitudinal and circular muscles (important for motility)
  • covered in shiny sirosa= waterproof layer which allows gut to move easily (slide over eachother)
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5
Q

Q: What is the mesentary? (3)

A

A: fan shaped

  • throws the small intestine in folds
  • holds SI in place
  • supports the blood supply
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6
Q

Q: Villi of the small intestine. Function? (2) Have? (3) Regulation?

A

A: -enormously increase the internal surface area
-villi are motile = create currents and maximise exposure to gut content

  • have a rich blood supply
  • have lymph drainage
  • have good innervation from submucosal plexus -> can regulate itself without needed brain input
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7
Q

Q: Which cells are in the small intestine? (5)

A

A: mucosa is lined with simple columnar epithelium consisting of:

  • primarily entercocytes (absorptive cells)
  • scattered goblet cells
  • enterendocrine cells

in crypts of lieberkuhn, epithelium includes:

  • paneth cells that have protective role
  • stem cells that replenish epithelium
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8
Q

Q: What is the main function of enterocytes? Direction? Shape? Structure? (4) What connects enterocytes? Lifespan?

A

A: absorption (apical ->basal)

tall columnar epithelia

  • microvilli on the apical surface= create brush border
  • nucleus sits towards the basolateral membrane
  • along with mitochondria
  • apical region of the cell is populated with rough endoplasmic reticulum

tight junctions

1-6 days

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9
Q

Q: What does the apical membrane of enterocytes have? Role? (3) Referred to as?

A

A: has a rich network of carbohydrates called the glycocalyx

  • helps to trap a layer of water, mucus and enzymes on the surface of the cell
  • protect it from the luminal contents (especially enzymes which may damage the cell/membrane),
  • to regulate digestion and absorption

layer is referred to as the ‘unstirred layer’

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10
Q

Q: What is goblet cell abundance? Shape? Structure? (5)

A

A: second most abundant cells in the small intestinal epithelium

goblet where it’s wider at top (upside down tear)

  • apical part of the cytosol is packed with mucin granules, which distorts the shape of the cell (like a goblet)
  • then GA
  • rER
  • nucleas with more GA
  • mito
  • curved point
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11
Q

Q: What does mucous consist of? Serves as? Why is it useful? Abundance?

A

A: water and glycoproteins

lubricant to facilitate gut passage

especially useful as water is constantly being absorbed from the lumen, which steadily dehydrates the contents

Because of this, the number of goblet cells increases along the entire length of the intestine (few in duodenum but many in colon)

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12
Q

Q: What are enteroendocrine cells? where? Shape? Structure? (5)

A

A: hormone secreting epithelial cells, most commonly found in the bottom of the crypts

roughly columnar but narrower apex

  • sensory apparatus is in the apical portion
  • mito
  • GA
  • nucleus (middle)
  • collections of manufactured hormones are kept near the basolateral membrane (ready to secrete into the local blood supply)
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13
Q

Q: Name 4 examples of enteroendocrine cells.

A

A: G-cells secrete gastrin

I-cells secrete cholecystokinin CCK

S-cells secrete secretin

D-cells secrete somatostatin

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14
Q

Q: What are paneth cells? where? (2) Priority role? (2) Contain? aka?

A

A: immunological cells

located at the bottom of the crypts near stem cells

protect these progenitor cells, as opposed to protecting the other cells of gut

  • they also engulf bacteria
  • regulate the intestinal flora

-high number of acidophilic granules (lysozyme granules)

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15
Q

Q: What do acidophilic granules contain? (3) Inc small description.

A

A: lysozyme: an antibacterial enzyme

glycoproteins: to protect local cells from enzymes
zinc: a common cofactor for lysozymes

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16
Q

Q: What’s the lifespan of enterocytes and goblet cells? Continually replaced by? feature?

A

A: very short lifespan of about 36 hours

stem cells from bottom of crypt= pluripotent

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17
Q

Q: How do stem cells grow (epithelia)? (3) Result? (3) Interference?

A

A: -proliferate in the crypts and ‘move up’ the sides of the villus towards the tip

  • Shortly after they reach the top they become senescent and naturally slough off
  • get broken down and reabsorbed

This is a continuous ‘escalator’ of birth, migration and death of epithelia.

If escalator-like transit of enterocytes is interrupted through impaired production of new cells (e.g. radiation) severe intestinal dysfunction will occur

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18
Q

Q: Why is there rapid turnover of enterocytes? (3)

A

A: -Enterocytes are the first line of defence against GI pathogens and may be directly affected by toxic substances in the diet.
- it is ‘easier’ to continually replace these cells than protect the huge numbers of cells at risk

-Any lesions will be short-lived.

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19
Q

Q: What does the cholera entertoxin do? (2) Treatment? Result? (2)

A

A: results in prolonged opening of the chloride channels in the small intestine allowing uncontrolled absorption of water

-leading to rapid, massive dehydration and death

rehydration-clean water and salts

Cholera bacteria will clear - epithelium will be replaced

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20
Q

Q: How is the duodenum distinguished? Role? where? Helps? (3)

A

A: first part of SI

Contains Brunner’s glands
=Coiled submucosal gland
-which secrete a bicarbonate-rich alkaline solution (mucous)
-which open up into the base of the Crypts

alkaline solution produced

  • Helps to neutralise acid chyme
  • protect the lining of the proximal small intestine
  • provide an optimum pH for enzymes
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21
Q

Q: How is the jejenum characterised? Compared to the rest of the small intestine? Appearance?

A

A: presence of large submucosal folds called plicae circularis

These are similar to the folds in the rest of the small intestine, but they are considerably taller, thinner and more abundant

They look much more like frills than folds.

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22
Q

Q: What does the ileum contain? Key to? Position? Ability? (2) Contain?

A

A: -up to 100 Peyer’s patches= aggregates of specialised lymphoid tissue = key to the immune response to gut-borne pathogens

well positioned to prevent bacteria from colon migrating up into small intestine

  • initiate leukocyte and immunoglobulin responses to pathogens
  • M-cells which do not have microvilli like the neighbouring enterocytes
23
Q

Q: What are the three main functions of intestinal motility? How are these functions achieved? (3)

A

A: 1. To mix ingested food with digestive secretions and enzymes-> digest effectively

  1. To facilitate the contact between contents and mucosal surface
  2. To propel the contents along the small intestine

via three mechanisms: segmentation, peristalsis and the migrating motor complex

24
Q

Q: What does segmentation result in? How? Duodenum and ileum comparison? Net movement?

A

A: -Mixes the contents of the lumen

  • occurs by stationary contraction of circular muscles at intervals
  • More frequent contractions in duodenum compared to ileum – allow pancreatic enzymes and bile to mix with chyme

Although chyme moves in both directions, net effect is movement towards the colon

25
Q

Q: What does peristalsis involve? (2) Net movement? minor effect?

A

A: -sequential contraction of adjacent rings of smooth muscle
-Most waves of peristalsis travel about 10cm (not the full length of the intestine)

  • Propels chyme towards the colon
  • minor effect is mixing

Most waves of peristalsis travel about 10cm (not the full length of the intestine)

26
Q

Q: What is the migrating motor complex? Fasting/fed state? Process? (3) Role? (2)

A

A: wave of contractions and electrical activity coming down the small intestine (sweeps through gut preventing accumulation of residue)

  • In fasting = cycles of smooth muscle contractions
  • Also occur in fed state – but less ordered and less frequent

Each cycle = contraction of adjacent segments of small intestine

  • Begin in stomach
  • migrate through small intestine towards colon
  • On reaching terminal ileum, next contraction starts in the duodenum

Prevents migration of colonic bacteria into the ileum and may ‘clean’ the intestine of residual food

27
Q

Q: Where are the secretions that facilitate digestion in the small intestine principally derived from? (4) Optimal condition? Where do enzymes tend to be effective? (2-inc location and where the E came from)

A

A: liver (and gall bladder), the pancreas and the small intestine wall

alkaline environment,

Enzymes tend to be effective at two sites:

  • Enzymes that cleave big nutrients into smaller nutrients operate in the gut lumen (usually released from glandular organs)
  • Enzymes that cleave dimeric nutrients into monomers for absorption are in the brush border of the enterocytes (usually released from the gut epithelium)
28
Q

Q: Where does the first stage of carbohydrate digestion occur? via? Where does sugar digestion not occur? Where does it occur after this? via? (2) What is the end goal?

A

A: in the mouth via salivary alpha amylase (but this is a minor effect) -> said E is destroyed in acidic stomach

no digestion of sugars in the stomach, and digestion resumes in the duodenum via pancreatic amylase and brush border enzymes.

The goal of digestion is to break the long/complex polymers into simple monomers that can be absorbed by the gut wall

29
Q

Q: In what environment does digestion occur in the small intestine? reason? (2) How do digestive enzymes enter? (2) Give an example. What else enters? via?

A

A: alkaline environment-> neutralise what’s coming in from stomach and optimise environment for enzymes

  • enzymes and bile enter duodenum via pancreatic duct and bile duct
  • duodenal epithelium also produce their own digestive enzymes eg. pancreatic alpha amylase

result is 2 layers of digestion- one in lumen via pancreatic enzymes (complex to disac and oligosac) and then at epithelium (to simple= that we can absorb)

30
Q

Q: Where does most carbohydrate digestion occur? Give 4 examples of simple carbohydrates. 3 complex.

A

A: small intestine

monosaccharides: glucose and fructose
disacc: sucrose and maltose (g+g)
complex = starch, cellulose, glycogen= sugars bonded to form chain

31
Q

Q: Compare primary active transport and secondary active transport. (3)

A

A: Both need carrier proteins and are against the gradient and require energy

  • primary uses energy from ATP hydrolysis
  • secondary uses energy from the electrochemical gradient (indirect source)
32
Q

Q: Where is pancreatic alpha amylase secreted into? response to? What does it allow? What does it need for optimal activity? (2) What provides one of these requirements?

A

A: duodenum in response to a meal

Continues digestion of starch and glycogen in the small intestine (started by salivary amylase)

Needs Cl- for optimum activity and neutral/slightly alkaline pH (Brunner’s glands in duodenum = alkaline secretion)

33
Q

Q: Give 3 examples of brush border carbo. enzymes?

A

A: maltase, lactase, sucrase

34
Q

Q: How are carbohydrates glucose and galactose absorbed? where? via? Describe.

A

A: through the apical surface by secondary active transport through the SGLT-1 transporter (Sodium Glucose Linked Transporter 1) - carrier protein and electrochemical gradient- provided by sodium (needs to stay low in cell)

The SGLT-1 transporters are supporters transporting one carbohydrate and one glucose into the cell at a time. Sodium is pumped out of the basolateral surface by a sodium potassium ATPase to ensure the sodium gradient.

35
Q

Q: How is carbohydrate fructose absorbed? via?

A

A: facilitated diffusion through GLUT-5 (GLUcose Transporter 5) channels

36
Q

Q: How are glucose, galactose and fructose also absorbed? where? via?

A

A: diffuse down their concentration gradient through the basolateral membrane using GLUT-2 channels

37
Q

Q: Where does protein digestion begin? via? What happens as it goes along GI tract? Where does digestion continue? Into? (2) Examples. (3) How are they secreted? Example.

A

A: Protein digestion begins in the stomach by pepsin, but pepsin is inactivated in the alkaline duodenum

Digestion continues in the duodenal lumen, where protease-rich pancreatic juice continues to break longer peptides into tripeptides and dipeptides. The pancreatic enzymes include trypsin, chymotrypsin and carboxypeptidase
-> secreted as precursors

Trypsin(=key) is activated by enterokinase, an enzyme located on the duodenal brush border.
Trypsin then activates the other proteases

38
Q

Q: Where does the final stage of protein digestion occur? by? Enzymes are typically? (2) Examples. (4)

A

A: in the brush border by enzymes secreted from the epithelial cells

typically tripeptidases and dipeptidases (i.e. they break down proteins 3 or 2 amino acids in length)

Specifically, these enzymes are endopeptidase, dipeptidase, aminopolypeptidase and carboxypeptidase.

39
Q

Q: What are digested proteins absorbed into in the small intestine? predominantly by? Specifically short peptides of 2/3 aa? (3)

A

A: Single amino acids are absorbed into enterocytes predominantly by secondary active transport through a variety of different transporters/ carrier proteins

absorbed via the apical surface where cytoplasmic peptidase enzymes breaks them down to amino acids prior to moving across the basolateral membrane into the blood via facilitated diffusion

40
Q

Q: Are lipids easy or difficult to digest? why? Process? (4)

A

A: -Lipids are poorly soluble in water, which makes them more complicated to digest

Four stage process in the small intestine

  • Secretion of bile and lipases,
  • Emulsification
  • Enzymatic hydrolysis of ester linkages,
  • Solubilisation of lipolytic products in bile salt micelles
41
Q

Q: Emulsification of lipids. What doesn’t mix? What is secreted into the stomach? at what point? What facilitates emulsification? into? What is the function of this? (2)

A

A: -Water and fat don’t mix.
-Bile and lipases are secreted into the duodenum

-Bile salts facilitate the emulsification of fat into a suspension of lipid droplets (~1m diam).

  • The function of emulsification is to increase the surface area for digestion.
  • Allows pancreatic lipase to split triglycerides
42
Q

Q: Where does the first stage of lipid digestion take place? with? Where does it continue? by? (2) how? How is the surface area of fats increased?

A

A: in the mouth where lingual lipase hydrolyses triglycerides

After swallowing, digestion continues in the stomach by ingested lingual lipase and secreted gastric lipase, which cleaves single fatty acid chains from free triglycerides

mechanical churning of the stomach slightly emulsifies the fats

43
Q

Q: Describe a bile salt molecule? (2) What are its 2 faces? What do they dissolve in?

A

A: Steroid nucleus planar- two faces. Amphipathic.

Hydrophobic (nucleus and methyl) face dissolves in fat

Hydrophilic (hydroxyl and carboxyl) face dissolves in water

44
Q

Q: What’s the structure of a bile salt micelle? Mixed micelles in small intestine? Function? -summarise.

A

A: Micelles = hydrophilic “head” regions in contact with surrounding solvent, sequestering the hydrophobic tail regions in the micelle centre

Mixed micelles in small intestine = water insoluble monoglycerides from lipolysis are solubilised by forming a core, stabilised by bile salts

digestion products reach the brush border and are combined with bile salts to form micelles, which are soluble enough to cross the aqueous unstirred layer so micelles are a way of escorting products of fat digestion-> brush border-> absorb effectively

45
Q

Q: What is the effect of lipase? Complex with? role? Without?

A

A: Lipase breaks down triglycerides into monoglycerides and free fatty acids- strips FA of 1 and 3 position

Pancreatic lipase complexes with colipase.

Colipase prevents bile salts from displacing lipase from the fat droplet-> without, lipase is less effective

46
Q

Q: Apart from pancreatic lipase, name 2 other important lipid enzymes. Include roles.

A

A: Phospholipase A2 hydrolyses fatty acids at the 2 position in many phospholipids, resulting in lyso-phospholipids (important for cell membrane/signalling molecules) and free fatty acids

Pancreatic cholesterol esterase hydrolyses cholesterol ester to free cholesterol and fatty acid

47
Q

Q: Where are lipids absorbed in the small intestine? How? What happens to the rest?

A

A: in the brush border

lipolytic products diffuse through the apical membrane and bile salts remain in the lumen (they travel through the small intestine and get reabsorbed in the terminal ileum to be reused- enterohepatic circulation)

48
Q

Q: What occurs to lipids once they have entered enterocytes in the small intestine? Pathways? (2)

A

A: monoglycerides and free fatty acids are resynthesised into triglycerides via two separate pathways.

primary mechanism is the monoglyceride acylation pathway,

secondary mechanism is the phosphatidic pathway (the details of these catabolic pathways are not essential information)

49
Q

Q: Describe monoglyceride acylation. (3)

A

A: 1. Fatty acids bind to the apical membrane.

  1. Fatty acid binding proteins (FABP) facilitate transfer of fatty acids from apical membrane to the smooth ER.
  2. In the smooth ER - fatty acids esterified into diglycerides and triglycerides.
50
Q

Q: Describe the phosphatidic pathway.

A

A: Triglycerides are synthesised from CoA fatty acid and alpha-glycerophosphate (ester of glycerol)

51
Q

Q: What happens to resynthesised triglycerides in enterocytes?

A

A: triglycerides are packaged with proteins, phospholipids and cholesterols into a lipoprotein called chylomicrons

-> taken to GA-> secreted across basement membrane via exocytosis

as they are too large to enter the capillaries, they enter the lymphatic system (via the villi’s lacteal)

52
Q

Q: What’s the composition of chylomicrons? (5)

A

A: 80-90% triglycerides, 8-9% phospholipids, 2% cholesterol, 2% protein, trace carbohydrate

53
Q

Q: What separates the ileum and the colon? How does it control passage of material? What does this also do?

A

A: ileocaecal sphincter

Relaxation and contraction controls the passage of material into the colon

prevents the back flow of bacteria into the ileum

54
Q

Q: Summarise:

  • carbohydrate digestion
  • protein digestion
  • lipid digestion
A

A: Carbohydrate digestion
-Pancreatic alpha amylase and brush border enzymes

Protein digestion
-Trypsin, which activates other proteases

Lipid digestion
-Emulsification by bile, hydrolysis and solubilisation into bile salt micelles

LSS Alimentary System (17 decks)

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