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Flashcards in Sem 4 molecules and mechanisms Deck (49):
1

Gastrin

Released from G cells in crypts of Liberkuhn (antral mucosa) response to stretching of stomach wall and presence of protein in stomach. Inhibited by secretin, CCK, GIP and somatostatin.
Function: activates ECL cells to secrete histamine, inc acid release from parietal cells. enhances activity of pyloric pump, promoting stomach emptying by inc gastric motility. Inc growth of gastric mucosa.

2

secretin

released from S cells in crypts of liberkuhn (duodenal mucosa) in response to gastric acid in duodenum - low PH. Stimulates release of watery bicarbonate ions from pancreatic and bile epithelium + in duodenum. reduces acid secretion from stomach by inhibiting gastrin release from g cells through somatostatin. stimulates pepsinogen from parietal cells. stim release glucagon insulin oancreatic polypeptide and somatostatin.

3

cholecystokinin CCK

released from I cells in duodenum and jejunal mucosa in response fatty substances and proteoses in chyme. Inhibits gastric emptying, reduces acid decretion from stomach by inhibiting gastrin release from G cells through somatostatin. stimulatess acinar cells of pancreas to release digestive enzymes, inc production of bile, contraction of gall bladder and relac sphincter of Oddi so bile delivered duodenum.

4

Gastric inhibitory peptide

releasaed from K cells in duo and jejunal mucosa in response to fatty substances and glucose in chyme. Weakly dec GI motility so weakly inhibits stomach emptying. Weakly reduces acid secretion from stomach by inhibiting gastrin release from G cells through somatostatin. stimulates insulin if hyperosmolarity of glucose in duodenum as incretin hormone.

5

GLP-1

released from L cells in duo and jejunal mucosa in respnce fatty substances and glucose in chyme. stimulate release of insulin if hyperosmolarity of glucose in duodenum as an incretin hormone.

6

somatostatin

released from D cells in crypts of Lieberkuhn (duo mucosa) and in pancreatic islets in response excess gastric acid in stomach and duodenum. inhibited by vagal stimulation. dec acid secretion by inhibiting G cells, ECL cells and parietal cells. dec pepsinogen sec. dec pancreatic and SI fluid secretion, dec gall bladder contraction thus reducing bile delivery to duodenum. Dec release of insulin and glucagon.

7

pepsinogen

released from peptic/chief cells in stomach, from stimulation of cells by Ach (vagal) and responce to acid. Inactive form of pepsin, activated into by HCL, pepsin is proteolytic enzyme that works in acidic conditions.

8

pepsin

activated from pepsinogen, activation inc by inc pepsinogen release. used in protein digestion

9

HCL

released from parietal/oxyntic cells in stomach, inc by histamine-ECL cells, Ach and gastrin. Inhibited by somatostatin, GIP, prostaglandinE2, Secretin. Makes the conditions in the stomach acidic. Allows breakdown of food.

10

intrinsic factor

released from parietal/oxyntic cells in stomach. Essential for absorption of vit B12 in distal ileum. It binds to vit b12 to protect from being digested in stomach, complex reaches terminal ileum where IF binds to receptor and vit b12 is absorbed. Autoimmune destruction of parietal cells leads to deficiency in intrinsic factor which can cause pericious anaemia.

11

bicarbonate ions

released from mucosal cells and brunners glands in duodenum. secretion inc by secretin. Inhibited by substance P. it neutralises acid and transported in mucus that covers gastric epithelium

12

mucus

released from mucous surface cells in stomach in responce to contact with food or iritation.

13

prostaglandin E2 PGE2

inhibited by NSAIDS like aspirin. Inc secretion of bicarbonate ions, dec acid secretion. Gi pathway. this is why can cause peptic ulcers as excess acid secretion.

14

histamine

released from ECL cells in responce to reduced acid secretion, secretion inc by gastrin and Ach. Inhibited by H2 receptor antagonists. increases acid secretion via H2 receptors on parietal cells. works via opposite intracellular pathway-Gs to PGE2 to inc acid.

15

trypsinogen

From acinar cells of pancreas, activated by enterokinase into trypsin. Inhibited by trypsinogen inhibitor. its the zygomen of trypsin, activated by enterokinase, activated autocatalytically by trypsin.

16

trypsin

result from activation of trypsinogen. stoped by trypsinogen inhibitor. Involved in protein digestion.

17

enterokinase

from the epithelial cells of intestine. activates trypsinogen into trypsin

18

chymotrypsinogen

released from acinar cells in pancreas. inhibited by trypsinogen inhibitor. inactive form of chymotrypsin, activated by trypsin.

19

chymotrypsin

result of activation of chymotrypsinogen. inhibited by trypsinogen inhibitor. protein digestion.

20

procarboxypolypeptidase

released from acinar cells of pancreas, inhibited trypsinogen inhibitor. inactive form of carboxypolypeptidase, activated by trypsin.

21

carboxypolypeptidase

as a result of activation of procarboxypolypeptidase. inhibited trypsinogen inhibitor. Protein digestion.

22

pancreatic amylase

released from acinar cells of pancreas. digestion (hydrolysis) of starches, digestion/hydrolysis of starches, glycogen and other carbs except cellulose to form mostly disaccharides and a few trisaccharides

23

pancreatic lipase

released from acinar cells of pancreas. Digestion (hydrolysis) of neutral fat into fatty acids and monoglycerides.
This is the main enzyme that caused the breakdown of fats, following emulsification

24

cholesterol esterase

released from acinar cells of pancreas. digestion/hydrolysis of cholesterol esters

25

phospholipase

released from acinar cells of pancreas. digestion of fatty acids to form phospholipids

26

trypsin inhibitor

released from acinar cells in pancreas. Prevents the activation of trypsin both inside the acinar cells and the ducts of the pancreas.
This prevents the digestion of the pancreas itself.
Dysfunction of trypsinogen inhibitor can cause acute pancreatitis.

27

lactase

released from enterocytes lining villi of SI. splits lactose into galactose and glucose.

28

sucrase

released from enterocytes lining villi of SI. split sucrose into fructose and glucose.

29

Maltase

Released from enterocytes lining villi of SI. split maltose into multiple molecules of glucose.

30

A-dextrinase

released from enterocytes lining villi of SI. split small glucose polymers into multiples molecules of glucose

31

peptidase (aminopolypeptidase) (dipeptidase)

In membrane of microvilli of brush border in SI. They split large polypeptides into tripeptides and dipeptides and a few into amino acids.
The breakdown products of polypeptides are transported through the microvillar membrane to the interior of the enterocyte.
There are more specific peptidases inside the enterocyte.
Once the peptides have been broken down into amino acids, they enter the blood from the basolateral membrane of the enterocyte

32

Lingual lipase

from lingual glands in mouth. Lingual lipase is swallowed with saliva into the stomach. It digests fats/triglycerides in the stomach.

33

bile salts and lecithin

found in bile. Emulsification of fats:
These surround fat globules.
These allow the globule to be fragmented into small, more water soluble globules.
This allows pancreatic lipase (a water soluble enzyme) to breakdown the fat globules into fatty acids and monoglycerides.
Bile salts form ‘micelles’ around these products and transport them to the brush border for absorption.

34

ras

Ras is involved in cell signalling.
Normally, it is bound to GDP and so inactive.
Upon binding with GTP, it becomes active.
Once active, it initiates a cell signalling cascade, leading to:
Inhibits apoptosis
Promotes cell growth
Promotes protein synthesis
Ras is an oncogene protein

35

Wnt (B catenin, APC, GSK-3B)

Wnt is a growth factor, involved in Wnt signalling.
When Wnt doesn’t bind to a cell, GSK-3B (and APC) keep B-catenin phosphorylated and so B-catenin is degraded.
When Wnt binds to the receptor on the cell, GSK-3B has no effect on B-catenin and so it is not phosphorylated and not degraded.
B-catenin can now enter the nucleus, cause transcription of Cyclin D, which then activates CDK4.
The cell has now entered the cell cycle.

36

cholesterol

produced by the liver. It is used in the formation of bile acids and salts.
Cholesterol is converted to primary bile acids in the liver, which is then transported to the duodenum via bile

37

bile acids/salts

produced by the liver and duodenum. Primary bile salts are synthesised from cholesterol.
They are transported to the duodenum via bile, where they undergo bacterial action and are converted into secondary bile acids.
Secondary bile acids conjugate into bile salts.
Bile salts cause emulsification of fats.

38

a keto acid

produced by the liver. Involved in transamination.
A keto-oxygen is transferred to an amino acid to make a new α-keto acid and a new amino acid.

39

ferritin/apoferritin

Iron is stored in the liver as ferritin.
Ferritin binds to apoferritin in the liver, which allows it to be stored.

40

Bilirubin, urobilinogen, urobilin, stercobilinogen, stercobilin

unconjugated-spleen. conjugated-liver. Bilirubin is a breakdown product of haemoglobin and is excreted in bile. RBC breakdown produces globin and heme. Heme is split into pyrrole nuclei, which are converted into biliverdin. Biliverdin makes unconjugated bilirubin. Unconjugated bilirubin is transported to the liver by binding to albumin. Hepatocytes take up unconjugated bilirubin and bind it with glucuronic acid/ sulfate, thus making it conjugated bilirubin. This travels to the duodenum in bile, where, under bacterial action, it is converted to urobilinogen. 90% of the urobilinogen is converted to stercobilinogen (under further bacterial action) and then into stercobilin, which is excreted in faeces. 10% of the urobilinogen is reabsorbed, across the intestinal epithelia. Some of the reabsorbed urobilinogen travels to the kidneys where it is excreted in urine as urobilin (after oxidation). Some of the reabsorbed urobilinogen travels back to the liver via the hepatic portal system

41

ABC transporters

found in liver and elswhere in body. 1. ‘A’TP ‘B’inding ‘C’assette transporter pumps.
2.These are dependent on the hydrolysis of ATP to allow active transport of molecules.
3.Examples include: Bile Salt Export Pump (BSEP)/ Multidrug Resistance Associated Protein 2 (MRP2) – both these are used to secrete primary bile acids fromhepatocytes into the bile canaliculi.

42

alanine transaminase ALT

produced in liver. 1. This is a transaminase enzyme, involved in the transamination process between Glutamine/Glutamate and Pyruvic Acid/Pyruvate to produce α-ketoglutamic acid/α-ketoglutarate acid and alanine

43

asparate transaminase AST

produced in the liver1. This is a transaminase enzyme, involved in the transamination process between Glutamate and Oxaloacetate to produce α-ketoglutarate acid and asparate.

44

alcohol dehydrogenase

priduced in stomach. metabolises alcohol in stomach. females lack it.

45

cytochrome p4502E1

in liver, involved in alcohol metabolism in liver, alcohol converted acetaldehyde and excreted by conversion to CO2 in citric acid cycle

46

cyclin

1. These activate CDKs by binding to them and acting as checkpoints throughout the cell cycle.

47

CDK cyclin dependant kinase

1.These are activated by binding to cyclins.
2.These are enzymes that serve as checkpoints throughout the cell cycle.
3.E.g. cyclinA/CDK4 and cyclinE/CDK2 and cyclinB/CDK1

48

cyclin kinase inhibitor

1. Inhibit CDKs and cause cell cycle to go into arrest.
2. E.g. p21

49

p53

1.In a normal cell cycle, p53 is degraded.
2.In an abnormal cell cycle, p53 is not degraded and it serves to kill the cell and prevent any abnormal tissue growing, by:
Inducing apoptosis
Causing cell cycle arrest by promoting p21 (CKI)
Blocking angiogenesis
Promoting DNA repair
3.P53 is a tumour suppressor gene protein. If both alleles of the gene that encodes p53 are mutated, then p53 can no longer induce DNA repair and apoptosis, thus the continuation of an abnormal cell cycle occurs.