Digestive

Front 1

FUnction of GI SYstem

Back 1

transfer organic nutrients, salts and water from the external environment to the internal environment

Front 2

Organization of the wall of the GI tract from stomach on

Back 2

MUCOSA
inner lumen lining - single layer of epithelium
Lamina propria - layer of CT
Muscularis Mucosa - smooth muscle
Submucosa - glands, submucosa plexus
MUSCULARIS EXTERNA
Circular smooth muscle
Myenteric nerve plexus
Longitudinal smooth muscle
SEROSA - CT

Front 3

Enteric Plexus

Back 3

Submucus plexus + Myenteric nerve plexus

controls neuronal activities of GI tract

Front 4

Chemical Digestion

Back 4

breaks down food with the use of enzymes
enzymes allow chemical bonds to be broken
proteins are broken down successively into:
proteins --> proteoses --> peptones --> polypeptides --> dipeptides --> amino acids

carbs/polysaccharides --> disaccharides --> monosac

Lipid --> fatty acids and glycerol (get the most energy from breakdown of fats

Front 5

Salivary amylase

Back 5

starts chemical digestion in the mouth
initiates carb digestion
secreted by the parotid salivary gland
optimum temp is 6.9 (same as the mouth)**Once food is swallowed Salivary amylase denatures and stops working due to change in pH

Front 6

Mucus

Back 6

mucopolysaccharide
Secreted by submandibular and subligual salivary glands
Mucus + serous fluid solution
Solution moistens and lubricates the food particles

Front 7

Bolus

Back 7

mass of food

Front 8

deglutition

Back 8

The act of swallowing the food
Bolus hits epiglottis
soft palate pushes up against nasopharynx
prevents food from entering nose

Front 9

Pharynx

Back 9

A. Oropharynx
B. laryngopharynx
C. contributes nothing to digestion
acts simply as a passageway

Skeletal muscle - involuntary!

Front 10

Esophagus

Back 10

doesnt contribute to digestion
is a passageway
transports food by peristalsis
ONLY open during swallowing
1st 1/3 = skeletal
2md 3rd = half/half
last 3rd = smooth muscle
stratified squamous Nonkeritinized epithelium
Muscularis = circular and longitudinal

Front 11

Stomach functions

Back 11

chemical breakdown of proteins
mechanicial breakdown by rugae

Front 12

7 types of cells lining the stomach

Back 12

1. chief: secrete pepsinogen
2. parietal: secrete HCL, secrete intrinsic factor
3. mucous cells: secrete mucus
4. Enterochromaffin-like (ECL) cells (found in stomach & intestines): secrete Histamine & serotonin as paracrine regulators of gastric secretion)
5. G cells secrete hormone Gastrin
6. D cells secrete the hormone Somatostatin (inhibits Gastrin secretion)
7. Stomach cells also produce a hormone called Ghrelin, which rises before meals and falls in levels secreted after meals. May be a signal to brain in order to regulate hunger.

Front 13

intrinsic factor

Back 13

necessary for vitamin B12 absorption by small intestine

secreted by parietal cells

Front 14

D Cells

Back 14

secrete Somatostatin (hormone)
inhibits Gastrin secretion

Front 15

Protein digestion

Back 15

begins in the stomach
Pepsin: initiates the protein digestion
Entrance of food in stomach stimulates the release of a hormone Gastrin from G cells into the blood, which causes the release of pepsinogen from other chief cells, and the release of HCl from parietal cells.
Pepsinogen is activated in presence of HCl --> Pepsin
Gastrin's ability to cause production of HCL is both direct (receptors on parietal cells for Gastrin) and indirect (Gastrin activates ECL cells which produce Histamine that binds to H2 receptors on Parietal cells causing release of HCL)

Front 16

Pepsin

Back 16

protease enzyme
breaks down proteins and is most active at pH 1.5-2.5
initiates protein digestion in the stomach

Front 17

HCl's 3 major functions

Back 17

1) activates inactive pepsinogen --> pepsin.

2) maintains ph of stomach between 1.5-2.5, so that pepsin can function optimally (and denaturation of proteins occurs)

3) Kills microorganisms which are ingested.

HCl production by Parietal cells is Activated by Gastrin directly and indirectly.
Direct: receptors on parietal cells for Gastrin
Indirect: Gastrin activates ECL cells which produce Histamine that binds to H2 receptors on Parietal cells causing release of HCl.

Front 18

Metabolic alkalosis

Back 18

If a person vomits frequently:
low HCl in stomach causes high HCl secretion by parietal cells --> high HCO3- going into the blood --> metabolic alkalosis

Front 19

Control of HCl secretion

Back 19

1. Cephalic stimulus: the sight, smell and taste of food stimulates the vagus PS nerve and the release of gastrin, which increases the secretion of HCl from parietal cells directly and indirectly
**HCl production before even the first bite.

2. Gastric stimuli: After swallowing a bolus, distension of hte stomach, a decrease in [H+] or peptides in the stomach causes the stimulation of the vagus PS nerve and the release of the hormone gastrin, both of which increases the secretion of HCl.

3. Intestinal Stimuli: like an anti-stimulus; in the small intestine, an increase in osmolarity due to chyme, an increase in [H+], or distension of the small intestine INHIBITS the vagus PS nerve and causes the release of GIP, both of which inhibit HCl secretion
***GIP also stimulates Insulin production

Front 20

Small Intestine

Back 20

3 regions

2 functions:
terminal digestion of food (involves pancreatic juice, bile and intestinal juice)
absorption of digested food

Front 21

Pancreatic juice

Back 21

composed of:
A. proteases (zymogens/precursors produced in pancreas, so as not to destroy Acinai cells of Pancreas)
1. trypsinogen
2. chymotrypsinogen
3. procarboxypeptidase
B. Amylases - break down carbs
C. Lipases - breakdown lipids into fatty acids and glycerol
D. Bicarbonate ion - neutralize acids that come from stomach

Front 22

Bile

Back 22

synthesized in liver
stored in gallbladder
facilitates the digestion of lipids
lowers the surface tension around the lipid molecules, emulsifies large lipids so that lipase enzymes can be exposed to more SA and break them down more rapidly --> mechanical, not chemical

Front 23

Intestinal Juice

Back 23

produced by the brush border cells & remain attached to the cells with active sites facing the intestinal lumen.
1. contains enterokinase
2. contains peptidases
3. contains disaccharidases
***includes sucrase, lactase and maltase
4. lipases : lipid digestion begins and ends in duodenum

Front 24

enterokinase

Back 24

converts trypsinogen to trypsin

Front 25

Disaccharidases

Back 25

Sucrase: breaks down sucrose into glucose and fructose
Lactase: breaks down lactose into galactose and glucose
Maltase: breaks down maltose into 2 glucose molecules

Front 26

Chyme enters Duodenum

Back 26

Secretin and CCK are released from cells of small intestine

Front 27

Secretin

Back 27

When Chyme enters the duodenum:
Gets secreted.
Goes to the pancreas and stimulates bicarbonate ion secretion into the duodenum, which neutralizes the acid from the stomach.
Goes to the liver and stimulates the secretion of bile, which emulsifies lipids aiding digestion.

Front 28

CCK

Back 28

When Chyme enters the duodenum:
Gets secreted.
Goes to the pancreas and causes the enzymes to be secreted into the duodenum.
Goes to the gallbladder and causes contraction of the gallbladder, releasing bile.

Front 29

Enterokinase

Back 29

When chyme enters the duodenum, CCK triggers pancreatic zymogens to be released into the small intestine.
Enterokinase, produced by the brush border cells, activates trypsinogen into trypsin,
trypsin activates chymotrypsinogen chymotrypsin
chymotrypsin activates procarboxypeptidase into carboxypeptidase

Front 30

Pancreatic Lipase

Back 30

Aided by bile which emulsifies the lipids.
Break down lipids: fatty acids and glycerol.
Lipid digestion begins and ends in the small intestine.

Front 31

Pancreatic Amylases

Back 31

Continue the digestion of carbs that was begun in the mouth by salivary amylase

Front 32

Water soluble vitamins

Back 32

Thiamine
Riboflavin
Pyridoxine
Ascorbic Acid

Front 33

Duodenum & Jejunum absorb:

Back 33

Iron
Calcium
Magnesium
Glucose
Disaccharides
Thiamine
Riboflavin
Pyridoxine
Ascorbic Acid
Amino Acids
Fat

Front 34

Ileum absorbs:

Back 34

Bile salts & water
Vitamin D, A, E, K ---- Fat soluble vitamins

Front 35

Large Intestine

Back 35

Major Functions: absorption and concentration.
The large intestine, mainly the colon, absorbs water, sodium, bicarbonate, calcium, magnesium, iron, several B complex vitamins, vitamin K and folic acid. All of this activity is heavily influenced by the bacteria present in the colon.

The other function of the large intestine is to concentrate the food which was indigestible, and those substances were not absorbed.

Front 36

Bacteria in colon

Back 36

numbers: 10^13-10^14
indigestable materials are broken down by these bacteria into short chain fatty acids that are used by the epithelial cells lining the colon to aid in absorption of sodium, bicarbonate, calcium, magnesium and iron

Front 37

Diverticulitis

Back 37

haustra divert
stick out, form pockets that trap fecal matter
surgical removal of pocket

Front 38

Cholera

Back 38

Enterotoxin (bacteria produce) stimulate active secretion of NaCl into lumen followed by osmosis.
Major diarrhea, can dehydrate to death.

Front 39

Celiac sprue

Back 39

damage to mucosa by Glutin (found in Wheat products)

Front 40

Lactose intolerance

Back 40

undigested Lactose in lumen encourages osmosis

Front 41

Gastrin

Back 41

Secreted by G Cells in stomach
Simuli for release are:
1. Peptides in the stomach
2. Distension of stomach
3. Decrease in H+ (acidity)
Stimulates acid secretion and enzyme secretion
Its secretion is inhibited by an increase in gastric secretion. (especially Pepsinogen from cheif cells)

Front 42

Secretin

Back 42

cAMP second messenger system
Released from small intestine
Stimulus for release is acid in the SI
Stimulates
1. bicarbonate secretion from the pancreas into the duodenum (neutralize)
2. bile secretion from the liver

Front 43

CCK

Back 43

Ca second messenger system
Released from the SI
stimulus for release is amino acid or fatty acids in the SI
Stimulates:
1. enzyme secretion from the pancreas into the duodenum (zymogens)
2. Contracts the gallbladder, releasing bile

Inhibits gastric motility

Front 44

Gastrin Inhibitory Peptide

Back 44

GIP
Glucose- Dependent Insulinotropic Peptide**: It's main function is actually to produce Insulin! New name.

Release from the SI
Stimulus for release is fatty acids or monosaccharides in small intestine
inhibits acid secretion in the stomach
Inhibits gastric motility
Stimulates insulin secretion from the Islets of Langerhans in response to glucose

Front 45

Gastric Motility

Back 45

When one swallows food, the vagus PS nerves are stimulated which relaxes the smooth muscle of the cardiac region of the stomach, in reception of food.
When food reaches the stomach, peristaltic waves of contraction occur in the stomach musculature, via vagus PS nerve stimulation.
Stimulus for gastric emptying is the distension of the stomach.
Inhibition of gastric emptying occurs when:
1. There is distension of the duodenum;
2. There is the presence of fat, acid, or hypertonic soln in the duodenum (fat most potent inhibitor)...causes stomach to slow its activity, stop unloading.
3. There is distension of the ileum (ileogastric reflex)

***Glucagon-like peptide-1 GLP-1, CCK, and Somatostatin all inhibit gastric activity and stimulates insulin secretion

Front 46

Small Intestine Motility

Back 46

1-4 cm section of SI contracts and relaxes and churns food in the tube. This is called Segmentation.
Stimulus for increased ileum contraction is gastric emptying (gastroileo reflex) - enteric nervous system
Fear decreases SI motility
Hostility increases SI motility.

Front 47

Segmentation

Back 47

1-4 cm section of small intestine contracts and relaxes and churns food in the tube.

Front 48

Large Intestine

Back 48

Has slow contractions
Material entering the large intestine may remain 18-24 hours
Stimulus for increased motility is eating via the gastroileal reflex - gastric emptying increases ileal motility, which moves material into the large intestine.
Stimulus for defecation is distension of rectum.

External anal sphincter:
last w/age
made of skeletal muscle
under voluntary control

Front 49

Defecation

Back 49

Assisted by:
deep inspiration
contraction of abdominal and chest muscles
** this increases intraabdominal pressure
** which increases pressure on the Large intestine
* defecation is also controllled by habit

Front 50

Secretin

Back 50

1 of the 2 hormones that gets released from small intestinal cells when Chyme enters the duodenum.
* goes to the pancreas and stimulates Bicarbonate ion secretion into the duodenum, which neutralizes the acid from the stomach
* goes to the liver and stimulates the secretion of bile which emulsifies lipids aiding digestion

Front 51

CCK

Back 51

Pancreozymin or Cholecystokinin
1 of the 2 hormones that gets released from small intestinal cells when Chyme enters the duodenum.
* goes to the pancreas and causes the enzymes to be secreted into the duodenum
* goes to the gallbladder and causes contraction of the gall releasing bile.

Front 52

Enterokinase

Back 52

Present in the intestinal juice, produced by brush border cells.
Activates Trypsinogen (from pancreas)
trypsin then activates chymotrypsinogen
Chymotrypsin activates Procarboxypeptidase into carboxypeptidase