Psl 301 Lec 30

Front 1

1) How much total digestion of fluid into GI and how much total input? How much reabsorption?

2) How is the body shaped to increase this reabsorption?

3) What are Rugae? What happens when stomach stretches

4) What is another mod to increase SA other than rugae?

s3

Back 1

1) 2 L food and drink input, 9 total input.

Most of 9 L reabsorbed

2) Microscopic protrusions on the tubes.

3) temporary folds of the lumenal surface of the stomach. When stomach stretches, they flatten out.

4) The gastric pits will lead to gastric glands,

Front 2

1) What are mods at the small intestine for increasing SA

s6

Back 2

1) -> Plica (Permanent folds in the small intestine, don't flatten out)

-> There are hills/valley shapes in Crypts of Lieberkuhn and villi, important for absorption. Microvilli are on epithelial cells, supporter by microfilaments keeping them erect.

Front 3

1) What are mods at the large intestine for increasing SA

s7

Back 3

1) -> Only have 3 bands of longitudinal muscles. Shorter than tissue of rest of large intestine. Tissue gets puckered up and get bulges. These are called Haustra, helping increase SA. Some are permenant, some are disappear and appear during mass movement.

-> Also have some valleys like Crypts of Lieberkuhn, and some invaginations. Not as much absorption as in small intesine cause less microvilli

Front 4

1) What happens in Celiac disease?

s8

Back 4

1) Immune response to glutin, get shortening of microvilli. Get malabsorption of material.

Front 5

1) What are the functions of the components of saliva

s9

Back 5

1) Function: Protection, lubrication, taste, digestion

Water (allows for contact of taste nerves with taste molecules, bicarbonate (protect from temp differences), mucus (trap bacteria), antibodies (IgA), Lysozyme (enzyme against bacterial cell wall), Defensins (Punch holes in bacterial cells), enzymes (salivary amylase by salivary glands, lingual lipase for fats)

Front 6

1) What are the 2 types of responses in salivation

2) What are the 3 salivary glands

s10

Back 6

1) -> Unconditioned response: Presence of food in mouth, mechano/chemo receptors to relay info to salivary center in medulla to cause release of saliva from salivary glands

-> Conditioned response: Doesnt need food in mouth; things like sight, smell or thought of food

2) Parotic, Sublingual, Submandibular

Front 7

1) What is the pathway for salivary

s11

Back 7

1) parasympathetic (lots of watery saliva): Neurons acting on salivary centre in medulla and pons -> efferent parasymp fibres acting on ganglia of various regions -> postganglionic fibres acting on salivary glands

-> Sympathetic (small amount of thick saliva): Neurons coming from spinal cord in the thoracic region acting on ganglia that innervate into the salivary glands

Front 8

1) What is secreted in the esophagus

2) What are the cell types in the stomach for secretion and what do they secrete

s12

Back 8

1) Not much, little bit of saliva

2) Gastric glands secrete a lot. Cells vary from region to region

Mucous cells: mucus, bicarbonate

Parietal cells: HCl, intrinsic factor

Chief cells: pepsinogen, gastric lipase

Enterochromaffin-like cells: histamine

D cells: Somatostatin

G cells: gastrin

Front 9

1) Where is mucus and bicarbonate secreted from and why are they important in stomach

s13

Back 9

1) -> secreted by mucus neck cells, and by mucus secreting cells on epithelial cells (called surface lining cells

->Mucus layer there because contents of stomach acidic, pH down low as 2. Physically protect epithelial cells from this.

-> The cells are also secreting bicarbonate, at the bottom layer of mucus, acting as a chemical barrier to protect epithelial cells from low pH

Front 10

1) What is Zollinger-Ellison syndrome

2) What do the parietal cells produce and what do they do. Describe the alkaline tide

s13,14

Back 10

1) Causes hyper acidity, causes damage to the mucus/bicarbonate barriers and damages the epithelial cells.

Due to gastrin secreting cells in pancreatic tumour.

2) Instrinsic factor: Bind to vitamin B12 (cobalamin), ensures absorption of vitamin B12 in ileum

Acid: kills bacteria, denatures protein, activates pepsinogen.

Have water as H+, coming from apical surface of parietal cells to the lumen. Cl- also builds up in parietal cells and goes into lumen, for net secretion of HCl. Cl and H+ combine in lumen.

The Cl- exchanger moves bicarbonate out of basolateral surface of the parietal cells. The bicarbonate goes to ISF and to blood, creating an alkaline tide. Can be measured, pH increases in that region of blood whenever ingest meal

Front 11

1) What do chief cells produce and what do they do

s15

Back 11

1) Pepsinogen: inactive form of pepsin, the acid activating it. Pepsin then can activate pepsinogen too. Then they can digest fats and collagens

Gastric lipase

Front 12

1) Where are G cells and what do they secrete and what do they do

s16

Back 12

1) G cells are in the pyloric end region of the stomach. Secrete gastrin. When peptides are present, gastrin released. Gastrin travels through bloodstream and activates cells in the body of stomach.

Gastrin binds to parietal cells receptors. Enhances secretion of HCl. Also binds to enterchromaffin-like cells, causes release of histamine. Histamine itself binding to parietal cells on lumenal surface can increase more HCl secretion.

Net effect: increase stomach utility, to cause mass movements e.g. reflexes in intestine.

Front 13

1) What pancreatic secretions enter the small intestine, and from what cells are they secreted from

s17

Back 13

1) Acinar cells: pancreatic amylase, pancreatic lipase, nucleases, inactive proteases (trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase,) etc.

duct cells: sodium bicarbonate and water

Front 14

1) How are pancreatic enzymes activated in the small intestine

2) What happens in the duct cells

s19

Back 14

1) By enterokinase (enteropeptidase) in the microvilli of the epithelium lining the duodenum. They activate stuff as the chyme moves around.

2) Duct cells secreting bicarbonate. In presence of Carbonic Anhydrase you get bicarbonate and H+. Bicarbonate moving out to the lumen, and also Cl- through the CFTR (cystic fibrosis transmembrane regulator). Now the H+ would go to blood and balances alkaline tide in blood.

Sodium and water also moves out to the lumen, get watery bicarbonate.

Front 15

1) Why do CF patients have to ingest pancreatic enzymes

s20

Back 15

1) Have to ingest pancreatic enzymes to ensure they can digest/absorb their nutrients.

Cause they have non functioning CFTR. dont have chloride and bicarbonate (cause no inbalance), and also dont have water drawn out. So mucus gets clogged up and the enzymes get collected here and dont get to duodenum.

Front 16

1) What is secreted from liver into small intestine via gall bladder

s21

Back 16

1) Bile: made of

-Bile salts

-lecithin

-cholestrol

-bilirubin

-bicarbonate

Front 17

1) Describe the Enterohepatic circulation

2) Describe cycle of bile/salt

Back 17

1) Primary bile acids synthesized by liver -> intestine -> hepatic portal vein -> liver -> cycle continues

2) Secondary bile acids: created by bacterial conversion in intestine

Bile acid convert to bile salt by conjugation with amino acids glycine or taurine. Released to duodenum through sphincter of oddi.

-Can have passive trasnport of bile salts anywhere but ineffective.

-Most have to modified by bacteria in terminal ileum. Then uncojugated back into bile acids back across epithelial barrier and into circulation and into liver

-Then continuous cycles of acid/salt through the day

Front 18

1) What hormones are released from small intestine

s23

Back 18

1) -Motilin from endocrine m cells. Released during fasting -> migrating motor complex

-GIP (Glucose-dependent insulinotropic protein): response to presence of glucose and fatty/amino acids to increase insulin.

-Secretin: by S cells in response to acid in duodenum. Incerasing release of bicarbonate in the pancreas to increase pH. Also reduces stomach activity and acid secretion.

-Cholecystokinin (CCK): by I cells in duodenum and jujenum, in response to fatty/amino acids. Enhances contraction of gall bladder. Bile helps digest fatty acids. Also increases release of pancreatic enzyme. Also reducing activity of stomach

-Glucagon-like peptide 1 (GLP-1): by L cells in ileum, in response to fatty acids and carbohydrates. Increase in insulin and decrease in glucagon. Beta cells proliferate. Decrease stomach activity, also signals the brain for satiety feeling.