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GastroIntestinal Physiology > Digestion and Absorption > Flashcards

Digestion and Absorption Flashcards

1
Q

Define Digestion

A

An orderly process to breakdown proteins, fats and complex carbohydrates, catalysed by digestive enzymes.

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2
Q

Define Absorption

A

Digestive products, vitamins, minerals & water taken across mucosa into blood and lymph.

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3
Q

What are the 3 pairs of Salivary Glands

A
  • sublingual glands (under tongue)
  • parotid gland (front ear)
  • submandibular glands (under jaw)
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4
Q

What is saliva composed of:

A

Saliva is composed of 2 major constituents: serous and mucinous components.

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5
Q

What is the Serous component of saliva?

A

Serous component carries out digestive function and has: water, electrolytes, enzymes, IgA

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6
Q

What is the Mucinous component of Saliva?

A

Mucinous lubricates; principally contains lubricating glycoproteins mucin.

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7
Q

The function of Saliva?

A

Saliva for Oral Hygiene
- Helps wash away pathogenic bacteria as well as food particles that provide their metabolic support;
- Saliva contains factors that destroy bacteria: thiocyanate ions and proteolytic enzymes;
- Lysozyme: attack the bacteria, aid the thiocyanate ions in entering the bacteria & digest food particles.
- IgA in saliva can destroy oral bacteria, including some that cause dental caries.

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8
Q

What is salivary secretion controlled by?

A

Autonomic nervous system
- parasympathetic nervous system is the primary physiological control of salivary glands
- ACh is released at parasympathetic nerve endings which stimulate muscarinic receptors & trigger saliva secretion.
- interruption of parasympathetic supply impairs salivation severely.

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9
Q

What are the 2 cell types involved in gastric secretions?

A

Parietal cells – HCL, Intrinsic factor
Chief cells – Pepsinogens and gastric lipase

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10
Q

What stimuli cause the parietal cells to secrete stomach acid?

A
  1. ACh: released by parasympathetic fibres in vagus nerve efferents which synapse with parietal cells
  2. Gastrin: released by G Cells present in the pyloric glands of the stomach
  3. Histamine: released by enterochromaffin cells which lie adjacent to parietal cells in the oxyntic gland
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11
Q

The regulation of pepsinogen secretion:

A
  • Via the chief cells
  • occurs in response to two signals:
    - stimulation of the chief cells by ACh released from the vagus nerves or from the gastric enteric nervous plexus
    - stimulation of chief cell secretion in response to acid in the stomach. stimuli directly induce stomach acid secretion by parietal cells
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12
Q

The phases of gastric secretion:

A
  1. Cephalic Phase- vagus; pepsin and acid production
  2. Gastric Phase- Gastrin-histamine production
  3. Intestinal phase- nervous and hormonal mechanisms
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13
Q

What is gastric secretion made up of?

A
  • HCl
  • Mucus
  • Pepsin
  • Chymosin
  • Triacylglycerol lipase
  • Intrinsic factor
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14
Q

What does the glands of the small intestine secrete into the bowel?

A

Digestive enzymes such as.,
- Aminopeptidase
- Dipeptidases
- α-Glucosidase
- β-Galactosidase
- Sucrose α-glucosidase
- Phospholipases

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15
Q

What is the role of the Pancreas in digestion?

A

The pancreas produces pancreatic juice for digestion:
- pancreatic acini secrete digestive enzymes
- ductile cells secrete a sodium bicarbonate solution

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16
Q

What controls the secretion of pancreatic juice:

A

Hormones:
- CCK
- Secretin
- ACh

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17
Q

What is the function of ACh, CCK and secretin?

A

ACh and CCK: stimulate the acinar cells to produce large quantities of pancreatic digestive enzymes but relatively small quantities of water and electrolytes

Secretin: stimulates secretion of large quantities of water solution of sodium bicarbonate by the pancreatic ductal epithelium

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18
Q

The regulation of Pancreatic exocrine secretions:

A

CEPHALIC PHASE:
- Stimulated by smell, taste, chewing & swallowing
- Mediated by Ach through vagus nerve
- 20% of pancreatic enzymes

GASTRIC PHASE
- Stimulated by proteins & gastric distension
- Mediated by vago-vagal reflex
- 5-10% of pancreatic enzymes

INTESTINAL PHASE:
- Stimulated by acid in chyme & fatty acids
- Mediated by secretin, CCK and vago-vagal reflex
- 70-75% of pancreatic enzymes & fluid

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19
Q

What causes the release of CCK and secretin?

A

Acid from the stomach releases secretin from the walls of the duodenum

Fats and amino acids cause the release of cholecystokinin

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20
Q

What are the 3 major components of the pancreatic exocrine solution:

A
  • water
  • digestive enzymes
  • sodium bicarbonate
21
Q

What are the 4 types of pancreatic digestive enzymes and their functions?

A

PANCREATIC AMYLASE: starch –> oligosaccharides
PANCREATIC NUCLEASES: RNA and DNA
PANCREATIC LIPASES: major triglyceride enzyme
PANCREATIC PROTEASES: trypsin, chymotrypsin, elastase

22
Q

What is bile secreted by:

A

Liver

23
Q

What are the 2 stages of bile secretion:

A

1st: secretion by hepatocytes into bile canaliculi; this contains bile acids, cholesterol, bilirubin & phospholipids.

2nd: secretion is made of water, bicarbonate, NaCl when by ductal epithelial cells are stimulated by Ach & Secretin

24
Q

What are the functions of bile:

A
  • bile salts & acids reduce surface tension and are responsible for the emulsification of fat for digestion and absorption.
  • eliminates waste products from blood in particular bilirubin & cholesterol (500mg of cholesterol converted to bile acids daily)
  • bile + pancreatic juice neutralises gastric juice as it enters the small intestine.
25
Q

Digestion of carbohydrates from the mouth:

A

IN MOUTH
– ingestion of food; chewing & swallowing
- salivary amylase starts to digest starch.

IN STOMACH
- Digestion continues for 1 hour via salivary amylase which converts starch to disaccharide (e.g. maltose).

IN DUODENUM:
- Secretin is released when low pH chyme (the partially digested food) enters duodenum
- this stimulates secretion of pancreatic fluid rich in HCO3- to neutralizes the chyme.

Pancreatic amylase hydrolyses most starch to disaccharides

Intestinal brush border enzymes breakdown disaccharides to monosaccharides

26
Q

What can a deficiency of one or more of the brush border cause:

A
  • Diarrhoea
  • Bloating
  • Flatulence after ingestion of sugar
27
Q

What is lactose intolerance

A

DEFINE: Inability to digest lactose effectively results in bloating, gas and diarrhoea.
- Intestinal lactase activity is high at birth but decrease in adulthood.
- Low level of lactase associated with intolerance to milk
- Incidence is common among blacks, Asians and Mediterranean

28
Q

What is the 4 types of lactase deficiency:

A
  • Primary lactase deficiency
  • Secondary lactase deficiency
  • Developmental lactase deficiency
  • Congenital lactase deficiency
29
Q

Where are the hexoses (oligosaccharides) absorbed?

A
  • small intestinal villi and microvilli
  • hexoses usually removed by the time the food reaches the ileum.
30
Q

What does the absorption of hexoses depend on?

A

Sodium ions in the intestinal lumen.

31
Q

Digestion of proteins:

A

IN STOMACH:
- Digestion begins in stomach by gastric juice:
- HCl activates pepsinogen, makes environment
suitable (pH2-3) for pepsin.
- Pepsin hydrolyses proteins to proteoses,
peptones and few polypeptides.
- pepsin has ability to digest collagen, a major
constituent of intercellular connective tissue of
meat.

32
Q

What are the 2 groups of proteolytic enzymes;

A

ENDOPEPTIDASES

EXOPEPTIDASES
- The carboxypeptidases of the pancreas are exopeptidases that hydrolyze the amino acids at the carboxyl ends of the polypeptides
- Trypsin, chymotrypsin, and elastase
- Attack the peptide bonds on the inside of a protein or peptide molecule, whereas the exopeptidases hydrolyze the terminal peptide bonds.
- Elastase digests elastin fibres that partially hold meats together.

33
Q

Absorption of proteins:

A
  • Small amount (2-5%) of the protein in the small intestine escapes digestion and absorption. Some are eventually digested by bacterial action in colon.
  • Peptides are absorbed together with a proton supplied by an Na+/ H+ exchanger by the peptide transporter 1.
  • Absorbed peptides are digested by cytosolic proteases, and any amino acids that are surplus to the needs of the epithelial cell are transported into the bloodstream by a series of basolateral transport proteins
  • A wide variety of dipeptides and tripeptides are taken up across the brush border membrane by the proton-coupled symporter known as PepT1. The proton gradient is created by the action of NA/H exchangers in membrane.
  • Cytosolic peptidases breakdown remaining linkage between amino acids in dipeptides and tripeptides
    Absorption of amino acids is rapid in the duodenum and jejunum but slow in the ileum.
34
Q

Digestion of lipids:

A

IN STOMACH:
- Up to 10% of fats (triglycerides) digested in stomach by lingual and gastric lipases.

IN SMALL INTESTINE
- First step is emulsification of large fat globules to very small sizes (in small intestine).
- Most fats digested in small intestine by pancreatic lipases.

IN DUODENUM:
- GB empties stored bile into the duodenum in response to CCK stimulus that itself is initiated by fatty food.
- Bile acts as an emulsifier, to allow water soluble pancreatic lipases act on them.
- bile salts, and especially lecithin are important in this role; making the fat globules easily fragmentable by agitation.
- Agitation produced by intestinal segmentation breaks fats into small droplets, 1µm in diameter
- Lecithin and bile salts coat small fat droplets to form micelles, exposing more surfaces for enzymatic action.
- Hydrophobic region of bile attracted to surface of layer of fat globules.
- Hydrophilic region projects into surrounding watery fluid, decreasing interfacial tension.

35
Q

Digestion by lipolytic enzymes:

A

Lipolytic enzymes in pancreatic juice include:
- Glycerol ester hydrolase
- cleaves 1st and 3rd fatty acids from triglyceride to
give 2 free fatty acids and 2-monoglyceride.
- Colipase
- required for Glycerol ester hydrolase binding to
surface of emulsion droplets in the presence of
bile acids.
- Cholesterol esterase
- cleaves ester bond in cholesterol ester to give 1
fatty acid and free cholesterol.
- Phospholipase A2
– cleaves ester bond at position 2 of
glycerophospholipid to give 1 fatty acid and 1
lysolecithin.

36
Q

What is the action of pancreatic lipase and how this affects absorption:

A

Pancreatic lipase will break down triglycerides to fatty acids and monoglycerides

The monoglycerides and FFA diffuse through the unstirred layer to the mucosal surface; then combined to form triglyceride in SER.

Monoglycerides, FFA, cholesterol and phospholipids diffuse across unstirred layer brush border membrane.

37
Q

Absorption of Sodium

A

Main drive for Na+ absorption is by active transport (Na-K-ATPase).
- Na+ leaves cell through the basolateral membranes into paracellular space
- this reduces Na+ concentration inside the cell, but creates electro- positivity in paracellular space.
- Cl- moves along this electrical gradient.
- Na+ moves down into the cell due to electrochemical gradient from the chyme; H2O follows.

38
Q

Absorption of water

A

Water:- daily intake of water ≈ 1.5 litres
- 7 litres fluid secreted into GI tract
- About 0.1 litre eliminated in faeces
> 8 litres water absorbed daily
- Net water absorption occurs mainly in small intestine: jejunum more active than ileum

39
Q

Absorption of bicarbonate:

A

large amount reabsorbed from upper small intestine indirectly

40
Q

Absorption of Calcium:

A

Calcium ions are actively absorbed into the blood especially from the duodenum.

amount absorbed controlled to supply exactly the daily need of the body for calcium.

30-80% of ingested calcium is absorbed.

PTH and vitamin D control calcium absorption

41
Q

Absorption of Vitamins:

A

Vitamins absorbed in Jejunum and Ileum:
- water-soluble:- absorbed by carriers Na+cotransporters in jejunum and upper ileum; (except B12 - in terminal ileum by IF)
- fat-soluble in jejunum:

42
Q

Absorption of Iron:

A

Iron is actively absorbed from the small intestine (duodenum).
- absorption is regulated by 3 factors:
- dietary intake;
- state of iron stores in the body,
- need for erythropoiesis.

Disorders of iron uptake can lead to anaemia or hemosiderin.

43
Q

What can cause malabsorption in the small intestine:

A

Several diseases can cause decreased absorption by mucosa; classified as Sprue
- Non-tropical sprue: this is variously called
- Idiopathic sprue
- Celiac dx (in children)
- Gluten enteropathy
- Tropical Sprue - frequently occurs in tropics
- It is believed to be caused inflammation of
intestinal mucosa as a result of unidentified
infectious agent

Early stages of sprue mainly impairs fat absorption leading steatorrhea
- Severe cases will impair absorption of proteins, carbohydrates, vit K, B12, folic acid calcium.

Removal of more than 50% of SI or a bypass could lead to malabsorption.
- Resection of ileum affects bile acids absorption.
- this leads to deficient fat absorption; then
diarrhoea
- Fat-soluble vitamins not absorbed adequately

44
Q

What can severe malabsorption lead to?

A

Severe malabsorption leads to:
(1) severe nutritional deficiency, often developing wasting of the body;
(2) osteomalacia (demineralization of the bones because of lack of calcium);
(3) inadequate blood coagulation caused by lack of vitamin K; and
(4) macrocytic anaemia of the pernicious anaemia type, owing to diminished vitamin B12 and folic acid absorption.

45
Q

What is absorbed in the large intestine and How:

A

Water and minerals.
- The large population of bacteria digest small amounts of fiber.
- Undigested residues are fermented by bacteria to SCFA.
- Bacterial activity forms: Vitamin K, Vitamin B12, Thiamin, Riboflavin, Biotin, and gases

How:
- Na+ enters the cell via ENaC channels and is transported to the interstitium through the Na+/K+ ATPase.
- Water and Cl-ions follow passively via the intercellular tight junctions to maintain electrical neutrality.

46
Q

What are the two common disorders of the large intestine:

A
  • constipation
  • megacolon
47
Q

What is constipation

A

Constipation: associated with dry, hard faeces in descending colon
- any pathology of LI that obstruct movement of intestinal contents leads to constipation; e.g. tumour, adhesions or ulcers.
- irregular bowel habits developed in lifetime of inhibition of normal defecation leads to constipation.

48
Q

What is Megacolon?

A

Megacolon: severe constipation with bowel movement only once in several day, sometimes a week
- large amount of faecal matter accumulate in colon causing distention
- Frequent cause of megacolon is lack or deficiency of ganglion cell in myenteric plexus

49
Q

Another name for megacolon?

A

Hirschsprung’s disease

GastroIntestinal Physiology (2 decks)

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