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Unit 10 lectures > Digestion and Absorption > Flashcards

Digestion and Absorption Flashcards

1
Q

Oral cavity components and digestive function

A

Teeth
- chewing

Salivary Glands
- lubrication
- salivary amylase
- salivary lipase

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2
Q

What is the digestive function of stomach?

A
  • Churning
  • Pepsins
  • Chymosin
  • Gastric lipase
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3
Q

Small intestine components and digestive function

A

Smooth Muscle
- churning
- propulsion

Pancreas
- trypsin
- chymotrypsin
- elastase
- pancreatic amylase
- pancreatic lipase

Gallbladder
- bile salts (stored in gallbladder)

Intestinal brush boarder
- aminopeptidase
- carboxypeptidase
- di-peptidase
- lactase
- sucrase
- maltase

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4
Q

Large intestine digestive function

A
  • Churning
  • Bacterial fermentation
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5
Q

What is absorbed in the small intestine?

A
  • water
  • Na+, K+, Cl-, Ca2+, Mg2+, Fe2+, vitamins
  • fatty acids
  • glycerol
  • cholesterol
  • amino acids
  • oligopeptides
  • monosaccharides (glucose galactose and fructose
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6
Q

What is absorbed in the large intestine?

A
  • water
  • Na+
  • K+
  • Cl-
  • vitamin K
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7
Q

What are the 3 phases of GI secretion?

A

Cephalic
- external enviroment and mouth

Gastric
- stomach

Intestinal
- intestines

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8
Q

What is the cephalic phase function? (4)

A

Prepares GIT to receive food:

  • lubrication with saliva
  • ensure acid is in stomach to kill bacteria
  • bicarbonate present to neutralise acid chyme escaping stomach
  • active enzymes in place for food arrival
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9
Q

Neural regulation of Cephalic phase (3)

A

1) PNS activated through sensory input from senses and cerebral cortex

2) Vagus nerve transmits PNS signals

3) PNS → ACh stimulates secretion from parietal cells, pancreatic duct and acinar cells

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10
Q

Hormonal regulation of Cephalic phase (3)

A

1) Food sensory input stimulates release of Gastrin-releasing peptide (GRP) from stomach

2) GRP stimulates gastrin release

3) Gastrin stimulates gastric acid secretion (preparing stomach for food)

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11
Q

What is ACh and Gastrin function in stomach?

A

Ach activates muscarinic cholinergic receptor (M3-R) on parietal cells to:
- secrete acid
- enterchromaffin cells, G cells

Gastrin release from G-cells in antrum activates:
- gastrin R on parietal cells to release acid
- Enterochromaffin-like cells to release Histamine
- which causes parietal cells to release acid
- D-cells release somatostatin, which inhibits parietal cells releasing acid

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12
Q

Mechanism of cephalic phase

A

1) sensory stimuli → vagus nerve

2) ACh → muscarinic cholinergic receptor → parietal cell → secrete acid

3) Gastrin release from G cells in antrum → gastrin receptors on parietal cells → acid secretion

→ enterchromaffin-like cells → histamine release → parietal cells → secrete acid

→ D cells → somatostatin → parietal cells → inhibits acid secretion

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13
Q

Function of Gastric phase (3)

A
  • enhance secretions started in cephalic phase
  • acidify chyme
  • initiated protein digestion
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14
Q

Neural regulation of Gastric phase (3)

A

1) food in stomach triggers stretch receptors in stomach wall

2) triggering Vagus nerve → medulla oblongata → stomach → activate ENS

3) ENS coordinates local reflexes → gastric secretions, motility and muscle contraction

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15
Q

Hormonal regulation of Gastric phase (3)

A

Gastrin is primary hormone responsible for gastric phase regulation

1) presence of food causes gastrin release by G cells

2) causing release of gastric acid by Parietal cells

3) and also pepsinogen by Chief cells

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16
Q

Mechanism of Gastric phase (7)

A

1) distension of stomach stimulates local ENS reflexes → stimulates ACh release

2) distension of stomach also stimulates Vagovagal reflex → stimulating release of ACh and GRP

3)
→ ACh activates Antral G cells, ECL cells and Parietal cells
→ GRP activates Antral G cells

4)
→ Antral G cells cause Gastrin release
→ ECL cells cause Histamine release
which activates Parietal cells.

5) Gastrin causes further activation of Parietal cells, Acinar cells, Chief Cell and Enterchromaffin cells.

6) Parietal cells secrete H+, which activates pepsinogen (which is released from activated chief cells) to pepsin.

7) Acinar cells cause release of pancreatic enzymes

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17
Q

Function of Intestinal phase

A
  • Control rate of chyme into duodenum
  • Maintain optimal conditions for enzymatic digestion
18
Q

Neural regulation of Intestinal phase (4)

A

1) Chyme in duodenum activates stretch receptors and chemoreceptors in intestinal wall

2) activating ENS and vagus nerve → medulla oblongata

3) medulla oblongata → activates enterogastric reflex

4) enterogastric reflex inhibits gastric motility and gastric secretion → slows emptying of stomach → ensures thorough digestion and absorption in small intestine

19
Q

What is the hormonal regulation of intestinal phase?

A
  • Cholecystokinin (by I-cells in duodenum)
  • Secretin (by S-cells in duodenum)
  • CCK released in response to fat and protein in duodenum → bile (from liver and gallbladder) and pancreatic enzymes → aid fat and protein digestion
  • Secretin released in response to acidic chyme in duodenum → pancreas secrete bicarbonate- rich pancreatic juice → neutralise acidic chyme
20
Q

What occurs in the duodenum during intestinal phase?

A

1) Acidic chyme stimulates the duodenal S-cells to release Secretin (pH <4.5):
→ stimulates duct secretion
→ HCO3- secretion from duodenal gland
→ inhibits H+ secretion by stomach parietal cells
→ constriction of pyloric sphincter

2) FA and peptones stimulate vagovagal reflex:
→ maintaining parasympathetic stimulation of acinar and duct cells

3) AA and peptones stimulates duodenal G-cells secrete Gastrin:
→ stimulates acinar cell secretion

4) FAs stimulate duodenal I-cells to release CCK (cholecystokinin):
→ relaxation of hepatopancreatic sphincter (to allow Oddi to release Bile from common bile duct)
→ contraction of gall bladder (to release concentrated Bile - to emulsify fats)

5) Bile salts assid lipid digestion:
→ emysifying lipid droplets
→ inc surface area for digestion

21
Q

IBD Mechanism (4)

A
  • dysregulated immune responses
  • chronic inflammation and ulceration of GIT
  • impairs secretions and absorption
  • malnutrition and GI symptoms
22
Q

GERD mechanism (5)

A
  • dysregulation of gastric acid secretion
  • inc production of stomach acid
  • flows into oesophagus
  • irritation and inflammation → GORD
  • heartburn, regulation, chest pain and complications like oesophagus, Barrett’s oesophagus
23
Q

Exocrine Pancreatic Insufficiency (EPI) mechanism (3)

A
  • insufficient secretion of pancreatic digestive enzymes and HCO3- into duodenum
  • impaired digestion and malabsorption of fats protein and carbs
  • steatorrhoea, weight loss and nutrient deficiencies
24
Q

Peptic ulcers mechanism

A
  • dysregulation acid secretion + infection with Helicobacter pylori bacteria or using NSAIDS
  • development of peptic ulcers
  • abdominal pain, bloating, bleeding and perforation
25
Q

How is Exocrine Pancreas controlled?

A

Bile and pancreatic juices flow into hepatopancreatic ampulla (HPA)

They exit into duodenum → controlled by hepatopancreatic sphincter (sphincter of Oddi)

26
Q

What does the Pancreatic Acinar cells release and how is auto digestion prevented?

A

Pancreatic acinar cells - enzyme secretion:
→ proteases, pancreatic lipase and amylase
→ isotonic fluid to carry enzymes (25%)

Pancreatic enzymes packaged in zymogen granules:
→ secreted upon stimulation of acinar cells
→ enzymes are inactive precursors of mature enzymes (preventing auto digestion)

27
Q

What do the Pancreatic Duct cells release?

A

→ HCO3- secretion
→ hypotonic fluid to carry enzymes (75%)

28
Q

How does the hormone secretin control pancreatic NaHCO3- secretion? (6)

A

1) acid in duodenum

2) ↑ secretin release by duodenal mucosa (S-cells)

3) stimulates pancreatic duct cells to

4) ↑ secretion of aqueous NaHCO3- solution into duodenal lumen

5) neutralisation

6) back to 1

29
Q

How does the hormone cholecystokinin (CCK) control pancreatic digestive enzyme secretion?

A

1) fat and protein in duodenum

2) ↑ CCK release from duodenal mucosa (I-cells)

3) stimulates pancreatic acinar cells to

4) ↑ secretion of pancreatic digestive enzymes as zymogens into duodenal lumen

30
Q

What are the components of pancreatic secretions and what are their functions?

A

Bicarbonate solution
→ optimise pH for pancreatic enzymes
→ protects small intestine

Lipase
→ hydrolyses TTG to monoglycerides and FFA
→ secreted in case [active] form

Amylase
→ converts polysaccharides to disaccharides, maltose
→ secreted in case [active] form

Proteolytic enzymes
→ Trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase
→ last 3 are all proenzymes (inactive) which hydrolyse protein into AA
→ secreted in case [inactive] form

31
Q

How are Proenzymes activated?
(Protein)

A

1) trypsinogen is cleaved by enteropeptidase in duodenal brush border to its active form Trypsin

2) then Trypsin cleaves more Trypsinogen to make more Trypsin

3) proenzymes release from pancreas

4) trypsin cleaves other proenzymes activating them

  • chymotrypsinogen → chymotrypsin
  • proelastase → elastase
  • procarboxypeptidase → carboxypeptidase
32
Q

How are Proenzymes activated?
(Lipase)

A
  • pancreatic lipase is secreted in active form
  • but is inefficient unless bound to Colipase

1) Trypsinogen → Trypsin

2) release of pancreatic Lipase and Procolipase

3) Procolipase → (+ trypsin) → Colipase binds to pancreatic Lipase → active pancreatic Lipase

33
Q

What causes of Auto Digestion?

What is there to prevent it?

What can it lead to?

A

Inappropriate Trypsin activation could lead to auto digestion.

Zymogen granule have acidic interior:
→ trypsin activity is greatest at alkaline
→ therefore stops Trypsin activity

Zymogen granules also contain serine protease inhibitors (SPINK1):
→ guards against auto digestion
→ loss leads to hereditary forms of pancreatitis

Pancreatitis → Loss of SPINK1 causes premature activation:
→ premature activation of pancreatic digestive enzymes
→ auto digestion of pancreatic tissue → ↓ secretion of digestive enzymes
→ compromised digestion and absorption of nutrients

34
Q

Pathophysiology of Pancreatitis

A

Obstruction:
→ due to gallstones, abnormal viscous mucous (cystic fibrosis), tumors cause pancreatic secretion back up

Acinar cell damage:
→ alcohol abuse
→ release of proteolytic enzyme into pancreatic tissue

Both obstruction and acinar cell damage lead to:
→ premature activation of intracellular trypsin in pancreatic acinar cells
→ causing autodigestion and inflammation

35
Q

Mechanism of HCO3- secretion

A

1) Duct cells:
CO2 converted to HCO3- and H+ by carbonic anhydrase

2) produced HCO3- is co-transported (into pancreatic duct) by anion exchanger

3)
→ cystic fibrosis transmembrane conductance regulator (CFTR) functions as an ion channel
→ allowing CL- across cell membranes and providing source of luminal Cl-
→ (Cl- to enter duct cell for a HCO3- out into lumen)

4)
→ Accumulation of Cl- causes Na+ and water to be reabsorbed back into lumen
→ (accumulation of luminal anions, so reabsorption down transepithelial osmotic and potential gradients)

5)
→ H+ accumulation prevented by Na+/H+ exchange allowing further CO2 to HCO3- conversion

H+ + HCO3- -> H2O + CO2

36
Q

What is Zollinger-Ellison syndrome?

A

Tumours (gastronomas) release gastrin:

  • causes stomach to release too much acid
  • peptic ulcer formation
37
Q

How are AA absorbed

A

Oligopeptidases such AA4 broken down by brush border petidase to AA3, which are transported via PepT1 from lumen to epithelial cells across basolateral membrane then broken down by tripeptidase to single AA that is then transported to interstitial space. Same thing occurs for AA3 to AA2 (dipeptidase instead) or AA2 to AA

(image)

  1. proteins + pepsin-> proteoses and peptones
  2. oligopeptides & short polypeptide -> brush boarder-> AA
  3. AA transporters->sodium coupled transporters across basolateral membrane

-loss of AA group/ mutation in AA transporter+ metabolic problems, growth and developmental defects

38
Q

How are monosaccharides absorbed

A

Disaccharides converted to monosacharides (disaccharidases on brush border membrane)
Glucose and galactose with Na+ transported across basolateral membrane from lumen to epithelium via SGLT1 and fructose via GLUT5. They are both then transported to interstitial space with GLUT2

(image)

  1. carbs + salivary amylase-> mono and disaccharides
  2. disaccharides on brush boarder-> monosaccharides
  3. glucose & galactose-> secondary active transport (SGLT1)
  4. fructose-> facultativo transport (GLUT5)
  5. monsaccharides-> blood (GLUT2)
39
Q

How are fatty acids absorbed

A

bile salts aggregate to micelles creating a polar surface on it allowing it to freely diffuse or fatty acid transporter (CD63) through brush border into lumen, which has a lower pH giving more chance of pronation.
then undergoe reesterfication reactions to form phospholipids, triglycerides and cholesterol in Smooth ER. They are then packaged in golgi into chylomicrons, which then goes into lymph and then blood.

  1. bile acids emulsify lipid droplets-> lipase breaks FA free from droplet
  2. lipase breaks down triacylglycerols-> FFAs-> mucosal lining
  3. mucosal lining dec pH from Na+ H+ exchanger= protonation of FAs
  4. FAs leave micelle-> enterocyte via fatty acid transporters(CD36) or direct diffusion-> new triglycerides-> released from chylomicrons-> lymph duct-> blood
40
Q

How is Iron absorbed

A

Fe3+ converted to Fe2+ via ferric reducatse at brush border, which is then transported via DMT1 to enterocyte. Fe2+ in heme is release via heme oxygenase. Some Fe2+ storred but mostly transported out of enterocyte via Ferroporin 1 on basolateral membrane. Hephaestin facilitates its transport from enterocyte to blood. In plasma Fe2+ converted to Fe3+ and bound to transferrin, where it is then transfered to bone marrow, liver. If iron overload hepicidin will bind to ferroportin to prevent Fe2+ binding.

1.ferric iron (Fe3+) reduced to ferrous iron by DCytB (duodenal cytochrome B)
2. Fe2+ is absorbed by DMT1 (divalent metal transporter )
3. intracellular iron is bound to mobiliferrin or converted to ferritin
4. Fe2+ transported into blood via ferroportin
5. Fe2+ oxidation back to Fe3+ by hephaestin
6. Iron is transported bound to transferrin
7. Haem iron- directly absorbed across brush boarder before release of iron by haemoxygenase

41
Q

How is lactase deficiency caused

A

Congential lactase deficiency
mutation in gene encoding lactase enzyme
Acquired lactase deficiency
dowregulation of lactase gene expressio due to people not drinking milk after weaning
both scenarios lead to dietry lactose not being broken down into glucose and galactose and it remains in the lumen. It has an osmotic forcecausing attraction of fluid leading to diarrhea. FLatulance also occurs due to fermentation of unabsorbed sugars by colonic bacteria

-lactase activity dec after weaning
- reduction is more extensive in some ethnic groups
-redcued ability to breakdown lactose into glucose and galactose
-no transporter for lactose
> gets retained in GIT
> osmotic diarrhoea
> bloating, abdominal pain, flactulence

42
Q

orlistat used for obesity

A

-inhibits pancreatic lipase
> prevents lipid absorption
> undigested triglycerides cannot cross the enterocyte membranes
> steatorrhoea (fatty dump)

Unit 10 lectures (14 decks)

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