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Semester 4 > Hormones and Molecules > Flashcards

Hormones and Molecules Flashcards

1
Q

Gastrin

  • Release
  • Inhibition of release
  • Effect
A

Release: From G cells in the crypts of Liberkuhn (antral mucosa) in response to stretching of the stomach wall and presence of protein food contents (amino acids) in the stomach

Inhibition: Secretin, CCK, GIP, Somatostatin

Effect:

  • activates ECL cells to secrete more histamine, thus increasing acid release from parietal cells
  • Enhances the activity of the pyloric pump, promoting stomach emptying by increasing gastric motility Increase growth of gastric mucosa
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2
Q

Secretin

  • Release
  • Effect
A
  • Release: from S cells in the crypts of Lieberkuhn (duodenal mucosa) in response to gastric acid in the duodenum (low pH in the duodenum)
  • Effect stimulates the release of:
    • water bicarbonate ions from pancreatic and bile epithelium and in the duodenum
    • reduces acid secretion from the stomach by inhibiting gastrin release from G cells through somatostatin
    • stimulates pepsinogen secretion from parietal cells
    • stimulates release of glucagon, insulin, pancreatic polypeptide and somatostatin
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3
Q

CCK - Cholecystokinin

  • Release
  • Effect
A
  • Release: from i cells in the duodenal and jejunal mucosa in response to fatty substances and protests in chyme
  • Effect:
    • Inhibit gastric emptying reduce acid secretion from stomach by inhibiting gastrin release from G cells through somatostatin
    • stimulates acinar cells of the pancreas to release digestive enzymes
    • Increases production of hepatic bile stimulates contraction of gall bladder and
    • the relaxation of the sphincter of Oddi resulting in the delivery of bile into the duodenum
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4
Q

Gastric Inhibitory peptide (GIP)

  • Release
  • Effect
A
  • Release: from K cells in the duodenal and jejunal mucosa in response to fatty substances and glucose in the chyme
  • Effect:
    • weakly decreases GI motility, thus weakly inhibits stomach emptying weakly
    • reduces acid secretion from the stomach by inhibiting gastrin release from G cells through somatostatin stimulates the release of insulin if there is hyperosmolarity of glucose in the duodenum as an incretin hormone
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5
Q

GLP-1

  • Release
  • Effect
A
  • Release: from L cells in the duodenal and jejunal mucosa in response to fatty substances and glucose in the chyme
  • Effect: stimulates release of insulin if there is hyperosmolarity of glucose in the duodenum as an incretin hormone
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6
Q

Somatostatin

  • Release
  • Inhibition of release
  • Effect
A
  • Release: from D cells in the crypts of Liberkuhn (duodenal mucosa) and in the pancreatic islets, in response to excess gastric acid in the stomach and duodenum
  • Inhibition of release: vagal stimulation -
  • Effect:
    • decrease acid secretion by inhibiting G cells, ECL cells and parietal cells
    • decrease pepsinogen secretion
    • decrease pancreatic and small intestine fluid secretion
    • decrease gall bladder contraction, reducing bile delivery to the duodenum decrease the release of insulin and glucagon
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7
Q

Pepsinogen

  • Release -
  • Effect
A
  • Release: from peptic chief cells in the stomach, due to stimulation of peptic cells by Ach vagal stimulation and also in response to acid in the stomach
  • Effect: this is the inactive form of pepsin, Activated into pepsin once it comes into contact with HCl, Pepsin is the active proteolytic enzyme that works in acidic conditions
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8
Q

Pepsin

  • Release
  • Effect
A
  • Release: result of activation of pepsinogen, activation increased by increased pepsinogen release
  • Effect: protein digestion
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9
Q

HCL

  • Release
  • Inhibition of release
  • Effect
A
  • Release: from parietal (oxyntic cells) in the stomach, secretion is increased by histamine (ECL cells) Ach and gastrin
  • inhibition of release:
    • somatostatin,
    • GIP,
    • prostaglandin E2 (PGE2)
    • secretin -
  • Effect: make the conditions in the stomach acidic by lowering the pH, this allows breakdown of food
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10
Q

Intrinsic factor

  • Release
  • Effect
A
  • Release: from parietal oxyntic cells in the stomach
  • Effect: essential for the absorption of B12 in the distal ileum, intrinsic factor binds to vitamin B12 in the stomach and protects it from being digested, the complex reaches terminal ileum and binds to receptors and B12 is absorbed.

Autoimmune destruction of parietal cells leads to deficiency in intrinsic factor which can cause pernicious anaemia

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11
Q

Bicarbonate ions

  • Release
  • Effect
A
  • Release: from mucosal cells
    • stomach
    • duodenum
    • salivary glands,
    • pancreas
    • Brunner’s glands (duodenum).
  • Secretion is increased by secretin
  • Inhibition of release: Substance P
  • Effect: Neutralise acid, bicarbonate ions are trapped in the mucus and cover the gastric epithelium
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12
Q

Prostaglandin E2 (PGE2)

  • Inhibition of release
  • Effect
A
  • Inhibition of release: NSAIDs e.g. Aspirin
  • Effect:
    • Increases the secretion of bicarbonate ions
    • Decreases acid secretion via the opposite intracellular pathway GI pathway to histamine to decrease acid secretion
    • This is targeted by NSAIDs e.g. aspirin and so can cause excess and secretion, leading to peptic ulceration
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13
Q

Histamine

  • Release -
  • Inhibition of release
  • Effect
A
  • Release: from ECL cells in response to reduced acid secretion, secretion increased by gastrin and Ach
  • Inhibition of release: H2 Receptor antagonists
  • Effect: Increases acid secretion via H2 receptors on parietal cells, works via the opposite intracellular pathway (Gs pathway) to PGE2 to increase acid secretion
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14
Q

Trypsinogen -Release - Inhibition of release - Effect

A

-Release: from acing cells of the pancreas, activated by enterokinase into trypsin - Inhibition of release: Trypsinogen inhibitor - Effect: Inactive form (zymogen) of trypsin, activated by enterokinase, activated autocatalytically by trypsin

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15
Q

Trypsin -Release - Inhibition of release - Effect

A

-Release: Ad a result of activation of trypsinogen - Inhibition of release: trypsinogen inhibitor - Effect: protein digestion

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16
Q

Enterokinase -Release - Effect

A

-Release: from the epithelial cells of the intestine - Effect: activates trypsinogen into trypsin

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17
Q

Chymotrypsinogen -Release - Inhibition of release - Effect

A

-Release: from acinar cells of the pancreas - Inhibition of release: trypsinogen inhibitor - Effect:inactive form (zymogen) of chymotrypsin activated trypsin

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18
Q

Chymotrypsin: -Release - Inhibition of release - Effect

A

-Release: activation of chymotrypsinogen - Inhibition of release: Trypsinogen inhibitor - Effect: Protein digestion

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19
Q

Procarboxypolypeptidase -Release - Inhibition of release - Effect

A

-Release: from acinar cells of the pancreas - Inhibition of release: trypsinogen inhibitor - Effect: inactive form (zymogen) of carboxypolypeptidase, activated by trypsin

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20
Q

Carboxpolypetidase -Release - Inhibition of release - Effect

A

-Release: as a result of activation of procarboxypolypetidase - Inhibition of release: trypsinogen inhibitor - Effect: protein digestion

21
Q

Pancreatic Amylase -Release - Effect

A

-Release: from acinar cells of the pancreas - Effect: digestion (hydrolysis) of starches, glycogen and other carbohydrates (except cellulose) to form mostly disaccharides and a few trisaccharides

22
Q

Pancreatic Lipase -Release - Effect

A

-Release: from acinar cells of the pancreas - Effect: Digestion (hydrolysis) of neutral fat into fatty acids and monoglycerides, this is the main enzyme that caused the breakdown of fats, following emulsification

23
Q

Cholesterol esterase: -Release - Effect

A

-Release: from acinar cells of the pancreas - Effect: digestion (hydrolysis) of cholesterol esters

24
Q

Phospholipase -Release - Effect

A

-Release: from acinar cells of the pancreas - Effect: digestion (hydrolysis) of fatty acids to form phospholipids)

25
Q

Trypsin inhibitor -Release - Effect

A

-Release: from acinar cells of the pancreas - Effect: 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

26
Q

Lactase -Release - Effect

A

-Release: from enterocytes lining the villi of the small intestine - Effect: split lactose into galactose and glucose

27
Q

Sucrase -Release - Effect

A

-Release: from the enterocytes lining the villi of the small intestine - Effect: splits sucrose into fructose and glucose

28
Q

Maltase -Release - Effect

A

-Release: from the enterocytes lining the villi of the small intestine - Effect: split maltose into multiple molecules of glucose

29
Q

alpha - dextrinase -Release - Effect

A

-Release: from the enterocytes lining the villi of the small intestine - Effect: split small glucose polymers into multiple molecules of glucose

30
Q

Peptidase (aminopolypeptidase dipeptidase) -Release - Effect

A

-Release: in the membrane of the microvilli of the brush border in the small intestine - Effect: 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 enterocytes once the peptides have been broken down into amino acids, they enter the blood from the basolateral membrane of the enterocyte

31
Q

Lingual Lipase

  • Release
  • Effect
A

Release: from lingual glands in the mouth

Effec:

  • Lingual lipase is swallowed with saliva into the stomach,
  • It digests fats/triglycerides in the stomach
32
Q

Bile salts (and Lecithin)

  • Release
  • Effect
A

Release: Found in bile

Effect:

  • Emulsification of fats
  • they surround fat globules
  • they 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 from micelles around these products and transport them to the brush border for absorption
33
Q

Alcohol Dehydrogenase

  • Release ​
  • Effect
A

Release: stomach

Effect:

  • Alcohol metabolism in the stomach
  • females have a lack of this enzyme, therefore their safe limits are lower than those in men
34
Q

Cytochrome p4502E1

Release ​

Effect

A

Release : Liver

Effect:

  • Alcohol metabolism in the liver
  • Alcohol is converted to acetaldehyde and excreted by conversion to CO2 in the citric acid cycle
35
Q

Cyclin

Function

A
  • Activate CDKs by binding to them and acting as checkpoints throughout the cell cycle
36
Q

Cyclin dependent Kinase (CDK)

Function

A
  • Activated by binding to cyclins
  • These are enzymes that serve as checkpoints throughout the cell cycle
  • E.g CyclinA/CDK4, cyclinE/CDK3 and cyclinB/CDK1
37
Q

Cyclin Kinase inhibitor (CKI)

A
  • Inhibit CDKs and cause cell cycle to go into arrest e.g. P21
38
Q

p53

A
  • In a normal cell cycle it is degraded
  • in an abnormal cell cycle it is not degraded and it serves to kill the cell and precent any abnormal tissue growing by:
    • inducing apoptosis
    • causing cell cycle arrest by promiting p21 (CKI)
    • Blocking angiogenesis
    • promoting DNA repair
  • P53 is a tumour suppressor gene. 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
39
Q

Ras

A
  • 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 intiates a cell signalling cascade leading to:
    • Inhibits apoptosis
    • promotes cell growth
    • promotes protein synthesis
  • Ras is an oncogene protein
40
Q

Wnt

(Beta - catenin)

(APC)

(GSK-3B)

A
  • Wnt is a growth factor involved in Wnt signalling
  • When wnt doesnt bind to a cell, SK-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 so it is not phosphorylated and not degraded
  • B catenin can npw enter the nucleus, cause transcription of Cyclin D which then activates CDK4
  • The cell has now entered the cell cycle
41
Q

Cholesterol

Release ​

Effect

A

Release : produced by the liver :

Effect:

  • 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
42
Q

Bile acids/salts

Release ​

Effect

A

Release: Produced in the liver and duodenum

Effect:

  • 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
43
Q

Alpha keto acid

Release ​

Effect

A

Release : Produced by the liver

Effect

  • Involved in transamintation
  • A keto-oxygen is transferred to an amino acid to make a new alpha keto acid and a new amino acid
44
Q

Ferritin/Apoferritin

Function

A
  • Iron is stored in the liver as ferritin
  • ferritin binds to apoferritin in the liver, which allows it to be stored
45
Q

Bilirubin

(Urobilinogen)

(Urobilin)

(stercobilinogen)

Stercobilin)

Release ​

Effect

A

Release ​

  • Unconjugated = spleen
  • conjugated = liver

Effect

  • Bilirubin is a breakdown product of haemoglobin and is extreted in bile
  • RBC breakdown produces globin and heme
  • Heme is split into pyrrole nuclei which are convreted 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 glucoronic 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 interstinal 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
46
Q

ABC transporters

Locatedd

Effect

A

Location: In the liver and elsewher in the body

Effect:

  • ATP Binding Cassette transporter pumps
  • These are dependent on the hydrolysis of ATP tp allow active transport of molecules
  • Examples inclue:
    • Bile salt export pump (BSEP)
    • Multidrug resistance associated protein 2 (MRP2)
  • Both these are used to secrete primary bile acids from hepatocytes into the bile canaliculi
47
Q

Alanine transaminase (ALT)

Release ​

Effect

A

Release : produced by the liver

Effect: A transmaninase enzyme involved in the transamination process between glutamine/glutamate and pyruvate to produce alpha ketoglutamic acid and alpha ketoglutarate acid and alanine

48
Q

Asparate transaminase (AST)

Release ​

Effect

A

Release : Produced by the liver

Effect: This is a transaminase enzyme, involved in the transamination processbetween glutamate and oxalacetate to produce alpha-ketoglutarate acid and asparate

Semester 4 (15 decks)

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