Wednesday, August 14, 2013
Phosphoglycerate Mutase
Glycolysis - (3PG) into (2PG)
Enzymes Enzymes Clinical Significance
Enzymes Enzymes Clinical Significance
Moves the phosphate position from 3C to 2C
Lyases- 3-phosphoglycerate Substrate
- Reversible
Additional Links:
Lipid Phosphatases
Require removal of phosphoryl groups of inositol lipids that had been phosphorylated as a part of signaling
Digestive System
Organ System
Cellular Metabolism CH13
Cellular Metabolism CH13
Function:
- Digestion of biomolecules, vitamins and inorganic minerals
Components/Anatomy:
- Gastrointestinal Tract Tissues
Organs/Anatomy:
- Mouth
- Esophagus
- Stomach
- Small Intestine
- Large Intestine
- Associated salivary glands
- Liver
- Pancreas
- Gall Bladder
Concepts:
- Digestion Path
- Vitamins
- Inorganic Minerals
Terminology:
- Digestion: breaking down food into progressively smaller particles and absorbed in the small intestine
- Biomolecules
Additional Information:
Pepsin
Digestive System
Proteolytic enzyme in the stomach converting polypeptdies into oligopeptides
Hydrolases- Activated Pepsinogen
Characteristics:
- Optimal activity in pH 1-2
LOC:
- Stomach
Concepts:
Additional Information:
Stomach
Digestive System
Primary organ of digestion that chemically processes biomolecules
Stomach
Fundamentals:
Characteristics/Specs:
- Located in the URQ
- Capacity for 2 L
- Gastric and pyloric glands
- Respond to signals from the brain activated by the sight, taste and smell of food
Function/Purpose:
- Processes biomolecules into chyme
- Combined mechanical and chemical digestive activities INC significantly Surface area of the food particles
- WHY? Optimize absorption
- Combined mechanical and chemical digestive activities INC significantly Surface area of the food particles
- 1)Proteins are denatured and degredation
- WHY?Denaturation renders protein a better substrate
- Stimulates Cholecystokinin (CCK)
- pH 1-2
- 2)Lipids are initially emulsified
Types of Secretions:
- Mucus
Salient Enzymes and Function Tests:
Enzymes:
- Pepsinogen - Pepsin
- Pepsin will digest proteins by cleaving peptide bonds near the aromatic rings resulting in short polypeptide fragments
- pepsin which is most active at pH of 2
Stomach Function Tests and Assessment:
Anatomy:
Gross Anatomy:
- Cardia/Cardiac/Gastroesophageal Sphincter
- Fundus
- Body
- Pylorus
- Pyloric Sphincter
Micro Anatomy:
Molecular- ATP dependent proton pump similar to Na K ATPase
- Mucus/Surface cells - secrete mucus
- Endocrine cells/Pyloric glands - secretes Gastrin
- Gastrin - stimulates secretion of HCl and Pepsinogen
- Activates Parietal cells and Chief Cells
- Gastrin - stimulates secretion of HCl and Pepsinogen
- Gastric pits
- Parietal cells - secretes HCl (pH 1)
- Activates acid initially activates Pepsinogen-Pepsin:ZYM for autocatalysis
- Prevents most known bact
- Chief cells - secretes Pepsinogen
Concept:
- Surface Area - MATH
- Enzymes - Zymogens/Proenzymes
Terminology:
- Gastric Pit: region where parietal cells and chief cells are located
- Chyme: acidic semifluid mixture
Additional Information:
Secretin
Digestive System
Small Intestine
When hydrochloric acid passes from the stomach into the duodenum, secretin is released into the bloodstream and stimulates the acinar cells of the pancreas to secrete water and bicarbonate into the pancreatic ducts that drain into the duodenum. By this mechanism, hydrochloric acid secreted by the stomach, which can be damaging to the intestinal lining, is promptly diluted and neutralized. Secretin also inhibits the secretion of gastrin, which triggers the initial release of hydrochloric acid into the stomach, and delays gastric emptying.
''Molecular basis''
Secretin increases watery bicarbonate solution from pancreatic duct epithelium. Pancreatic acinar cells have secretin receptors in their plasma membrane. As secretin binds to these receptors, it stimulates adenylate cyclase activity and converts ATP to cyclic AMP. Cyclic AMP acts as second messenger in intracellular signal transduction and leads to increase in release of watery carbonate. It is known to promote the normal growth and maintenance of the pancreas.
It counteracts blood glucose concentration spikes by triggering increased insulin release from pancreas, following oral glucose intake.
Although secretin releases gastrin from gastrinomas, it inhibits gastrin release from the normal stomach. It reduces acid secretion from the stomach by inhibiting gastrin release from G cells. This helps neutralize the pH of the digestive products entering the duodenum from the stomach, as digestive enzymes from the pancreas (e.g., pancreatic amylase and pancreatic lipase) function optimally at slightly basic pH.[citation needed]
In addition, secretin stimulates pepsin secretion from chief cells, which can help break down proteins in food digestion. It also stimulates release of glucagon, pancreatic polypeptide and somatostatin.
Stimulates the pancreas to release of sodium bicarbonate
PancreasSecretin
Fundamnetals:
- Stimulated by from low duodenal pH (2-4.5)
- Also the secretion of secretin is increased by the products of protein digestion bathing the mucosa
- Also bile salts and fatty acids
- Oligopeptide stimulated
Function/Purpose:
- Target organ Pancreas
- Secrete bicarbonate
- Enhances CCK's function
LOC:
- Small intestine - duodenum
Additional Information:
Secretin is a hormone that causes pancreatic juice to be excluded from the pancreasWhen hydrochloric acid passes from the stomach into the duodenum, secretin is released into the bloodstream and stimulates the acinar cells of the pancreas to secrete water and bicarbonate into the pancreatic ducts that drain into the duodenum. By this mechanism, hydrochloric acid secreted by the stomach, which can be damaging to the intestinal lining, is promptly diluted and neutralized. Secretin also inhibits the secretion of gastrin, which triggers the initial release of hydrochloric acid into the stomach, and delays gastric emptying.
''Molecular basis''
Secretin increases watery bicarbonate solution from pancreatic duct epithelium. Pancreatic acinar cells have secretin receptors in their plasma membrane. As secretin binds to these receptors, it stimulates adenylate cyclase activity and converts ATP to cyclic AMP. Cyclic AMP acts as second messenger in intracellular signal transduction and leads to increase in release of watery carbonate. It is known to promote the normal growth and maintenance of the pancreas.
It counteracts blood glucose concentration spikes by triggering increased insulin release from pancreas, following oral glucose intake.
Although secretin releases gastrin from gastrinomas, it inhibits gastrin release from the normal stomach. It reduces acid secretion from the stomach by inhibiting gastrin release from G cells. This helps neutralize the pH of the digestive products entering the duodenum from the stomach, as digestive enzymes from the pancreas (e.g., pancreatic amylase and pancreatic lipase) function optimally at slightly basic pH.[citation needed]
In addition, secretin stimulates pepsin secretion from chief cells, which can help break down proteins in food digestion. It also stimulates release of glucagon, pancreatic polypeptide and somatostatin.
Small Intestine
Digestive System
Secretes chemicals and primary location of absorbing biomolecules
Small Intestine
Fundamentals:=
- Bulk of chemical digestion
- Chemicals (Intest&Panc) are the key to proper digestion and absorption
- Important in mechanical digestion of lipids
Function/Purpose:
- Biomolecule Absorption
- Secretion of CCK
- Biomolecule Synthesis
- Lipid resynthesis of triacylglycerides from fatty acids and monoacylglycerols
Salient Enzymes and Function Tests:
Enzymes:
- Enteropeptidase/Enterokinase/Master Switch
- Activates trypsiogen and trypsin
- Secretin
- Cholecystokinin (CCK) - secreted
- Triggers the release of Bile into the small intestine
- Triggers the release of Pancreatic Juice
- Maltase - converts maltose into glucose
- Surface of intestinal cells
- alpha-Glucosidase - digests maltotriose and other oligosaccharides
- Surface of intestinal cells
- Sucrase - digests sucrose (GLU and FRU) disaccharide
- Surface of intestinal cells
- Lactase - converts lactose into GAL and GLU
- Dipeptidase - cleave the peptide bond of dipeptides to release the AA’s
Stomach Function Tests and Assessment:
Anatomy:
Gross Anatomy:
- Duodenum - most digestion occurs
- Illeum
- Jejunum
Micro Anatomy:
- Inner Wall
- Villi
- Microvilli
- Villi
- Epithelial Cells
- Blood Vessels
- Lymphatics
- Circular Muscle
- Longitudinal Muscle
- Smooth Muscle
Regulation:
- PNS-ANS inhibits the digestion
Concept:
- Pancreatic Juice - Pancreas
- Biomolecules
- Surface Area and Convolutions
- Volume - Surface area and Length
- Tissue difference btwn Small and Large Intestines
- Nervous System
- Endocrine System
- Peristalisis and Endocrine and Nervous System
- Endocrine
- Hormones influence epithelial and endocrine cells
- Nervous System
- Parasympathetic Nervous System - innervates the peristalisis
- electrical continuity imposed by Gap Junctions of circular & longitudinal muscles
- Parasympathetic Nervous System - innervates the peristalisis
- Endocrine
Terminology:
- Peristalisis: quick and unconscious gastrointestinal contractions of Smooth Muscle
Additional Information:
Cholecystokinin
Digestive System - Small Intestine
Stimulates pancreas and gall bladder to secrete digestive enyzmes and bile salts
Pancreas Gall BladderCholecystokinin (CKK)/Gastrin
- Clincal values
Function/Purpose:
- Stimulated by initial digestion products in stomach
Tissue source:
Diagnostic significance:
Assay for enzyme activity:
Source of error:
Additional Information:
Zymogens
[[Enzymes]]
==Precursors of enzymes==
====Function/Purpose:====
====Salient Examples:====
*[[Pepsinogen]]
*[[Chymotrypsinogen]]
*[[Trypsinogen]]
*[[Procarboxypeptidase]]
*[[Proelastase]]
====Additional Information:====
==Precursors of enzymes==
====Function/Purpose:====
====Salient Examples:====
*[[Pepsinogen]]
*[[Chymotrypsinogen]]
*[[Trypsinogen]]
*[[Procarboxypeptidase]]
*[[Proelastase]]
====Additional Information:====
Pepsinogen
Cellular Metabolism
Zymogen of Pepsin
PepsinPepsinogen
- Clinical values
Function/Purpose:
- Small amount of enyzme activity to activate itself to some degree in acidic environment
Tissue source:
Diagnostic significance:
Assay for enzyme activity:
Source of error:
] Temp: ENZ
] Temp: Organ
Medical Science - back
asdf
linksOrgan
Function/Purpose:
Salient Enzymes and Function Tests:
Enzymes:
Organ Function Tests and Assessment:
Anatomy:
Gross Anatomy:
Micro Anatomy:
Concept:
Additional Information:
Enteropeptidase
Enzymes
Digestive System
Digestive System
Enteropeptidase/Enterokinase
- Clincal values
Function/Purpose:
- Activates Trypsinogen-->Trypsin
Tissue source:
Diagnostic significance:
Assay for enzyme activity:
Source of error:
Additional Information:
Trypsin
Digestive System
Along with Enteropeptidase, activates Trypsinogen to form Trypsin
TrypsinogenTrypsin
- Clincal values
Function/Purpose:
- Master switch of the pancreatic zymogens
Tissue source:
Diagnostic significance:
Assay for enzyme activity:
Source of error:
Additional Information:
Gall Bladder
Digestive System
Secretes bile salts produced in the liver
LiverFunction/Purpose:
- Primary lipid emulsification - Bile Salts
Salient Enzymes and Function Tests:
Enzymes:
Organ Function Tests and Assessment:
Anatomy:
Gross Anatomy:
Micro Anatomy:
Concept:
Diseases:
- Cholelithiasis - common
- Cholecystisis - common
- Cholangiocarcinoma
Procedures:
Additional Information:
Snake Venom Poisoning
ConditionsDiseases List
Snake Venom Poisoning
Fundamentals:
- 50-60 proteins that vary from species to species
- Enzymes that digest cell membranes
- EX: Phospholipases
- Brake phospholipids and destroy phospholipids of skeletal muscles exposing insides of cells
- ER, mitochondria, nuc env membrane, plasma membrane all contain phospholipids
- Target the RBCs = hemolysis
- EX: Collagenases
- Digest collagen - connective tissue
- EX: hyaluronidase
- DIgest glycosaminoglycan - connective tissue
- Both destroy tissue at the site of the bite enabling the venom to spread more readily throughout the victim
- EX: Proteases
- Degrade basement membranes and components of extracellular matrix = severe tissue damage
- Stimulate formation of blood clotts as well as digest blood clots
- Neurotoxic activities
- Immobilize prey while the digestive enzymes take effect
Concepts:
Additional Information:
Med School
So here is the start of yet another project...
FYI DO NOT BOTHER APPYING TO PUERTORICAN SCHOOLS
Example #1 University of San Juan - From Gladys H. Gonzalez Navarrete MD JD
Carribean/Mexico
Australia
United Kingdom
Essay Samples
- [http://www.accepted.com/medical/sampleessays.aspx
- Will post up personal statements in future
Medical Schools
United States- Allopathic Medicine - MD
- Roughly 130+ schools
- Osteopathic Medicine - DO
- Roughly 30 schools
They maybe cheap but that's because of their preference for PR residents
pic comming soon"We appreciate your interest in our school, however, we must inform you that as a state-supported school, priority is given to residents of Puerto Rico. Due to this fact, we are unable to consider your application."Does not specify any out of state slots in the letter, will have to dig the MSAR.It states a "mr/NonResRejCta" in the very bottom of the letter so im not sure if there is a "mr/NonResAccCta" for acceptances but thats my 2 cents
Carribean/Mexico
- Roughly 22 schools
- - Ross University - Carribean School1
- There are Fall, Spring and Summer cycles
- St George's University - Carribean School2
- There are Fall and Spring cycles
- Carribean School3
- There are Fall, Spring and Summer cycles
- http://www.iime.org/database/pacific/philippines.htm
- http://www.upcm.ph/2007/admission.html -UP
- http://officialweb.upm.edu.ph/schoolsandcolleges.php
- http://www.flinders.edu.au/medicine/sites/medical-course/international-applicants/
- http://www.internationaldoc.com/
- http://nmatfordummies.blogspot.com/2010/03/frequently-asked-questions.html
Australia
United Kingdom
- - uk schools
- [1]
- http://www.google.com/#sclient=psy&hl=en&q=admissions+test+BMAT&aq=f&aqi=g-m1g-v1&aql=&oq=&pbx=1&bav=on.1,or.&fp=6ec3191c2b79d4d0
- http://www.ucl.ac.uk/medicalschool/mbbs-admissions
- http://www.ukcat.ac.uk/
- http://www.ukcat.ac.uk/pages/details.aspx?page=ukCatUniversities
- http://www.iime.org/database/europe/uk.htm
Regulation of Enzymes
Enzymes - back
Molecular perspective in the involuntary control of our biological catalysts
Regulation of Enzymes
Fundamentals
- Enzymes produce a product
Types of Inhibition:
Reversible Covalent Modificaiton- Allosteric Modulation
- Feedback
- Instantaneous
- Competitive Inhibition
- Noncompetitive Inhibition
- Uncompetitive Inhibition
- Suicide Inhibition
- Transition State Analog
Concepts:
- Bufers - Chemistry
Regulation of Metabolism
Cell Metabolism
Compartamentalizaiton
Controling Flux
Involuntary control of our body's energy functions
Regulation of Metabolism:
Function/Purpose:
- Products or reactants need to be in balance for our well being
Types of Regulation:
Coupled Reaction- a spontaneous reaction provides the energy needed by a nonspontaneous one
Compartamentalizaiton
- Hormonal
- Segregates opposed reactions
- Energy Charge - ADP Buffer
- (ATP + .5ADP)/(ATP + ADP + AMP)
- 1= all ATP
- 0= all AMP
- (ATP + .5ADP)/(ATP + ADP + AMP)
- Phosphorylation Potential
- ATP/(ADP + Pi)
Controling Flux
Concepts:
Additional Information:
Cell Metabolism
Cellular Metabolism - CH14
Nucelotide Metabolism
Complex Lipid Metabolism
Lipid Metabolism
Energy Metabolism
Cofactor Vitamin Metabolism
Other Amino Acid Metabolism
Other Substances Metabolism
The body's involuntary functions of vital energy reactions (anabolism and catabolism)
- Daily reactions we take for granted but necessary to function properly
Fundamentals:
Regulation of MetabolismGeneral Types of Pathways
- Linear: continuous series of reactions in which the product of one reaction is the reactant in the next
- Circular: series of reactions where the final product is an initial reactant
- Spiral: series of repeated reactions used to break down or build up a molecule
Biomolecule Metabolism/Intermediary/Central Metabolism:
Complex Carbohydrate Metabolism- Glycogen Metabolism
- Glucose Metabolism
- Pyruvate Metabolism
- Glycerol Metabolism
- Fructose Metabolism
- Galactose Metabolism
- Lactose Metabolism
- Sucrose Metabolism
- Pentose Phosphate Pathway
- Cellular Respiration
- (Aerobic Respiration)
- Glycolysis
- Pyruvate Decarboxylation - can be considered last step of glycolysis before TCA
- TCA Cycle
- Electron Transport Chain
Nucelotide Metabolism
Complex Lipid Metabolism
Lipid Metabolism
Energy Metabolism
Cofactor Vitamin Metabolism
Other Amino Acid Metabolism
Other Substances Metabolism
Concepts:
Terminology:
- Orthophosphate
- Anabolism: build up of chemicals to synthesize new products
- Catabolism: breakdown of chemicals to degrade into new products
- Intermediary/Central Metabolism: discrete pathways of one function
Additional Information:
GLC t G6P
Glycolysis
Glucose + ATP <-(Hexokinase)->>> Glucose 6-phosphate + ADP + H
HexokinaseFundamentals:
- Glucose is transported by specific transport proteins into the cell
- Glucose is phosphorylated by ATP to form Glucose 6-phosphate
- Phosphorylation changes polarity of glucose
- keeps the molecule inside the cell, does now allow the passage out of the membrane
- Phosphoryl groups destabilize glucose
- sets up an isomerization of the 6C structure
- Phosphorylation changes polarity of glucose
Specifics
- Hexokinase has two lobes that move toward each other
- Removal of water form the active site enhances the specificity of the enzyme
- Binding site could attack the gamma phosphoryl group of ATP forming ADP and Pi
Hexokinase
Glycolysis - GLC into (G-6P)
Phosphorylates glucose
TransferasesHexokinase
- Requires Mg
- Glucose substate
- Reversible reaction (favors product)
- Requires ATP
Additional Information:
G6P t F6P
Glycolysis
Glucose 6-phosphate <-(Phosphoglucose isomerase)-> Fructose 6-phosphate
Phosphoglucose isomeraseFundamentals:
- Glucose (aldose) is changed into Fructose (ketose)
- Only three carbon molecuels are metabolized and this makes it easier to cleave into the 3C fragments
Specifics
- Galactose is funelled through this step in Glycolysis
Additional Information:
G6P t F1,6BP
[[Glycolysis]]
==Glucose 6-phosphate <-(Phosphoglucose isomerase)-> Fructose 1-6-bisphosphate==
[[Phosphoglucose isomerase]]
====Fundamentals:====
*Glucose (aldose) is changed into Fructose (ketose)
**Only three carbon molecuels are metabolized and this makes it easier to cleave into the 3C fragments
====Specifics====
==Glucose 6-phosphate <-(Phosphoglucose isomerase)-> Fructose 1-6-bisphosphate==
[[Phosphoglucose isomerase]]
====Fundamentals:====
*Glucose (aldose) is changed into Fructose (ketose)
**Only three carbon molecuels are metabolized and this makes it easier to cleave into the 3C fragments
====Specifics====
PG Iase
Glycolysis -
(G-6P) into (F-6P)
Isomerizes phosphoglucose
IsomerasesPhosphoglucose Isomerase
Fundamentals:
- Glucose 6-phosphate substate
- Reversible reaction
- Enediol Rearrangement - OCHEM!
Additional Information:
GLC t G6P
[[Glycolysis]]
==Glucose + ATP <-(Hexokinase)-> Glucose 6-phosphate + ADP + H==
[[Hexokinase]]
====Fundamentals:====
*Glucose is transported by specific transport proteins into the cell
*Glucose is phosphorylated by ATP to form Glucose 6-phosphate
**Phosphorylation changes polarity of glucose
***keeps the molecule inside the cell, does now allow the passage out of the membrane
**Phosphoryl groups destabilize glucose
====Specifics====
*Hexokinase has two lobes that move toward each other
*Removal of water form the active site enhances the specificity of the enzyme
*Binding site could attack the gamma phosphoryl group of ATP forming ADP and Pi
==Glucose + ATP <-(Hexokinase)-> Glucose 6-phosphate + ADP + H==
[[Hexokinase]]
====Fundamentals:====
*Glucose is transported by specific transport proteins into the cell
*Glucose is phosphorylated by ATP to form Glucose 6-phosphate
**Phosphorylation changes polarity of glucose
***keeps the molecule inside the cell, does now allow the passage out of the membrane
**Phosphoryl groups destabilize glucose
====Specifics====
*Hexokinase has two lobes that move toward each other
*Removal of water form the active site enhances the specificity of the enzyme
*Binding site could attack the gamma phosphoryl group of ATP forming ADP and Pi
G6P t F1,6BP
[[Glycolysis]]
==Glucose 6-phosphate <-(Phosphoglucose isomerase)-> Fructose 1-6-bisphosphate==
[[Phosphoglucose isomerase]]
====Fundamentals:====
*Glucose (aldose) is changed into Fructose (ketose)
**Only three carbon molecuels are metabolized and this makes it easier to cleave into the 3C fragments
====Specifics====
====Additional Information:====
*[http://en.wikipedia.org/wiki/Fructose_1,6-bisphosphate Wikipedia]
==Glucose 6-phosphate <-(Phosphoglucose isomerase)-> Fructose 1-6-bisphosphate==
[[Phosphoglucose isomerase]]
====Fundamentals:====
*Glucose (aldose) is changed into Fructose (ketose)
**Only three carbon molecuels are metabolized and this makes it easier to cleave into the 3C fragments
====Specifics====
====Additional Information:====
*[http://en.wikipedia.org/wiki/Fructose_1,6-bisphosphate Wikipedia]
PFKase
Glycolysis - (F-6P) into (F-1,6BP)
Phosphorylates fructose
TransferasesPhosphofructokinase (PFK)
KEY ENZYME IN GLYCOLYSIS
- Requires Mg or Mn?
- Fructose 6-phosphate Substate
- Reversible reaction (favors product)
- Requires ATP
- Allosteric enzyme
Concepts:
Additional Information:
F6P t F1,6BP
Glycolysis
Fructose 6-phosphate + ATP <-(Phosphofructokinase)->>> Fructose 1-6-bisphosphate + ADP + Pi
Phosphofructokinase (PFK)Fundamentals:
- ATP required
- This addition of another ATP sets up enough energy to allow to cleave the 6C structure
Specifics
Additional Information:
F1,6BP t GAP + DHAP
Glycolysis
Fuctose 1,6-bisphosphate <-(Aldolase A)-> Glyceraldehyde 3-phosphate and Dihydroxyacetone phosphate
Aldolase AFundamentals:
- Reverse Aldol Reaction - OCHM!
Concepts:
- Aldol Chemistry]] - OCHM
Specifics:
Aldolase
Glycolysis - (F-1,6BP) into (GAP) + (DHAP)
Enzymes
Enzymes
Cleaves aldols
LyasesAldolase
- Fructose 1,6-bisphosphate Subtrate
- Reversible
Types:
- Aldolase A, B, C
Aldolase A
Aldolase B
Additional Information:
DHAP t GAP
Glycolysis
Dihydroxyacetone phosphase <-(Triose phospahte isomerase)-> Glyceraldehyde 3-phosphate
Triose phosphate isomerase3PIase
Glycolysis - (DHAP) into (GAP)
Converts the three sugar ketose into an aldose
IsomerasesTriose phosphate isomerase (TPI/TIM)
- Dihydroxyacetone phosphate Substatrate
- Reversible
GAP t 1,3BPG
Glycolysis - Gluconeogenesis
Glyceraldehyde 3-phosphate + NAD <-(Glyceraldehyde 3-phosphate dehydrogenase)-> 1,3,bisphosphoglycerate + NADH + H
Glyceraldehyde 3-phosphate dehydrogenase (GAPDH)General:
- Aldehyde is oxidized to COOH
- COOH is phosphorylated as NAD is reduced
- This sets up the molecule to generate ATP
- Unfavorable formation of a mixedanhydride - phosphorylated carboxylic acid
Specifics:
GA3PDHase
Glycolysis - (GAP) into (1,3BPG)
Enzymes - Enzymes Clinical Significance
Enzymes - Enzymes Clinical Significance
Oxidizes Glyceraldehyde 3-phosphate
OxidoreductasesGlyceraldehyde 3-phosphate dehydrogenase (GAPDH)
- Glyceraldehyde 3-phosphateSubstrate
- Needs NAD+
- Reversible
- Product has a high phosphoryl transfer potential
- Mixed anhydride of phosphoric acid and carboxilic acid
Coupled RXN Specifics:
- Oxidation of aldehyde to COOH by NAD
- Farovarble dG(o') -50kJ
- Joining of COOH and orthophosphate to form acyl-phosphate product
- Unfavorable
Concepts:
- Redox Chemistry - CHM
Additional Links:
Oxidoreductases
[[Enzymes]] - back
==catalyze an oxidation reduction between two substrates==
==EC1: Oxidoreductases==
====Salient Examples:====
*[[Drug Metabolizing Enzymes]] Cytochrome P450
*[[(GAPDH)]]
==catalyze an oxidation reduction between two substrates==
==EC1: Oxidoreductases==
====Salient Examples:====
*[[Drug Metabolizing Enzymes]] Cytochrome P450
*[[(GAPDH)]]
1,3BPG t 3PG
Glycolysis
1,3-bisphosphoglycerate <-(Phosphoglycerate Kinase)-> 3-phosphoglycerate
Phosphoglycerate KinasePhosphoglycerate Kinase
Glycolysis - (1,3BPG) into (3PG)
Enzymes
Enzymes
Dephosphorylates 1,3BPG and creates ATP
Transferases- 1,3-bishposphoglycerate Substrate
- Reversible
- Creates ATP
- Substrate level phosphorylation
Additional Links:
Pyruvate Decarboxylation
Cell Metabolism
Combustion of pyruvate into Acetyl-CoA
LOC:
- Mitochondria - mitochondrial matrix
Summary:
- Pyruvate + CoA into AcCoa
- Pyruvic acid + Coenzyme A into Acetyl-CoA
- Requires NAD
- Produces CO2 and NADH
- Pyruvic acid + Coenzyme A into Acetyl-CoA
Steps:
- Pyruvate is brought into the mitochondrial matrix
- Transporter protein
- Commits pyruvate to become Acetyl-CoA
- Transporter protein
- Pyruvate Dehydrogenase Complex (3 enzymes + 5 coenzymes)
3PG to 2PG
Glycolysis - Gluconeogenesis
Phosphoglycerate Mutase
Phosphoglycerate Mutase
3-phosphoglycerate <-(Phosphoglycerate Mutase)-> 2-phosphoglycerate
Glycolysis2-phosphoglycerate <-Phosphoglycerate Mutase)-> 3-phosphoglycerate
GluconeogenesisMechanism:
General- Phosphorylation and dephosphorylation
- NOT an intermolecular attack of the alcohol with the phosphate
- WHY? - educated guesses
- Enzyme holds the molecue at a particular shape
- Enzyme has an affinity = rate that revents intermolecular attack
- Steric hindrance of the 2O(-)s means that there is an extra electron (6 total) repelling
- Environment is slighlty basic pH of 7.3-ish so this allows the Os on the phoshate to remain deprotonated
- To me since there is resonance, it seems like the steric
hindrance is further intensified by the "swatting" of the O atom as it
converts from a singe tetrahedral configuration to a planar carbonyl.
- Imagine that the three Os are all in resonance periodically "swatting" away the chances for an intermolecular attack
- MAYBE the concept of a feris wheel and mini golf put puts
- each O as it swats away the chance of OH intermolecular attack
- WHY? - educated guesses
- NOT an intermolecular attack of the alcohol with the phosphate
PGate Mase
Glycolysis - (3PG) into (2PG)
Enzymes Enzymes Clinical Significance
Enzymes Enzymes Clinical Significance
Moves the phosphate position from 3C to 2C
Lyases- 3-phosphoglycerate Substrate
- Reversible
Additional Links:
Enolase
Glycolysis - (2PG) into (PEP)
Enzymes Enzymes Clinical Significance
Enzymes Enzymes Clinical Significance
Dehydrates to 3C to form a double bond or the enol of the soon to be keto
Lyases- 2-phosphoglycerate Substrate
- Reversible
Additional Information:
2PG t PEP
Glycolysis - Gluconeogenesis
Enolase
Enolase
2-phosphoglycerate <-(Enolase)-> phosphoenolpyruvate
GlycolysisPhosphoenolpyruvate <-(Enolase)-> 2-phosphoglycerate
GluconeogenesisDetails:
- Phosphoryl traps PEP in its unstable enol form
OAA t PEP
Gluconeogenesis
- Addition of phosphoryl group is highly unfavorable, Glycolysis
- Carboxylation and decarboxylation are much more favorable, Gluconeogenesis
- Decarboxylations often drive reactions that are otherwise highly endergonic
Heme Synthesis
Glycine and Succinyl-CoA to create heme
Mitochondria, Cytoplasm- Alanine (5-aminolaevulinic acid) synthesis – Glycine and Succinyl-CoA condensation
- Alanine Synthase – controls of porphyrins and heme synthesis rate, controlling enzyme
- Porphobilinogen (PBG) subunit synthesis – Two alanines combine to form monopyrrole ring PBG
- Alanine Dehydratase – DEC = ALA dehydratase porphyria
- Hydroxymethylbilane synthesis – Four PBGs combine to form linear tetrapyrrole—four monopyrroles strung together end to end
- Hydroxymethylbilane Synthase/PBG Deaminase – DEC = acute intermittent porphyria (AIP).
Uroporphyrinogen lll Four of the carboxylic acid side chains (COOH) are successively knocked off by the enzyme uroporphyrinogen decarboxylase (UROD), producing the heptacarboxylic, hexacarboxylic and pentacarboxylic porphyrinogen intermediates (not shown), ending in coproporphyrinogen lll. This enzyme is defective in porphyria cutanea tarda (PCT).
Coproporphyrinogen lll A further two carboxylic acid side chains are knocked off by the enzyme coproporphyrinogen oxidase, which is defective in hereditary coproporphyria (HCP).
Protoporphyrinogen lX This molecule is then oxidised from protoporphyrinogen lX to protoporphyrin lX by the enzyme protoporphyrinogen oxidase, which is defective in variegate porphyria.
Protoporphyrin lX An iron atom (Fe2+) is inserted into the centre of the tetrapyrrole ring to form heme. This is catalysed by the enzyme ferrochelatase, which is defective in erythropoietic protoporphyria.
HEME BREAKDOWN
The tetrapyrrole ring is broken open (See the gap between the O atoms at the top of the structure below).
This step is catalysed by the enzyme heme oxygenase.
Biliverdin This is further reduced to bilirubin by the enzyme biliverdin reductase
Bilirubin Bilirubin is the form in which the breakdown products of heme are excreted from the body: in the bowel, it is further broken down to urobilinogen and stercobilinogen by bacteria.” – from additional info Capetown
Salient Chemicals:
- Glycine
- Succinyl-CoA
- Alanine synthase
- Alanine
Additional Information:
- Rensselear Polytechnic Institute
- Universities of Cape Town – South Africa ty Dr. Vaso Lykourinou-Tibbs
Tuesday, August 13, 2013
PEP t Pyruvate
Glycolysis
Phosphoneolpyruvate + ADP <-(Pyruvate Kinase)->Pyuvate + ATP
Pyruvate KinasePyruvateAdditional Information:
Pyruvate Kinase
Transfers Pi from sugar to ATP
Glycolysis - (2PG) into (PEP)Enzymes Enzymes Clinical Significance
Kinases
- Phosphoenolpyruvate Substrate
- Ireversible
Additional Information:
Pyruvate
Pyruvate/Pyruvic Acid
Cell Metabolism
Function/Purpose:
- Variable and verastile compound
Fundamentals:
Fate of pyruvate is variable:- 1)Can be converted into acetaldehyde --> Ethanol
- 2)Can be converted into lactate
- 3)Can be converted into Acetyl CoA --> Carbon Dioxide and Water
- 4)Can be convterted into oxaloacetate --> Free GLC or Glycogen
Concepts:
- Compound vs Molceule - defs
- Carboxylic Acids
Terminology:
- Fermentations are ATP generating process in which organic compounds act as both donors and acceptors of electrons
FRU 1P Path
Fructose 1-phosphate Pathway
Conversion of Fructose in the liver to be metabolized by Glycolysis
Liver
Fructose
Glycolysis
- Fructose into Fructose 1-phosphate
- Fructose 1-phosphate into 1)Dihydroxyacetone Phosphate (DHAP) and 2)Glyceradehyde
- Fructose 1-phosphate Aldolase/Aldolase B
- Mechanism is via the formation of a Schiff Base
- 1)DHAP goes into stage 2 of Glycolysis
- 2)Glyceraldehyde into Glyceraldehyde 3-phosphate
- Triose Kinase
- GAP goes into stage 3 of Glycolysis
- Triose Kinase
Concepts:
- Schiff Base Chemstry]] - OCHM
FRU
Fructose
Ketose sugar
Carbohydrates - Carbohydrate List
Cell Metabolism
Fructose Metabolism:
Additional Information:
GAL
Galactose
Aldose sugar
Carbohydrates - Carbohydrate ListCell Metabolism
Galactose Metabolism:
- There is no dedicated pathway to catabolize Galactose like Glucose/Glycolysis
- They are funneled as intermediates
- Can be degraded via GAL-GLC Interconversion Pathway
Conditions/Diseases:
Additional Information:
GAL-GLC Int Path
Galactose
Galatcose-Glycose Interconversion Pathway:
- Converts Glactose into Glucose 6-phosphate (G-6P)
- Galactose + ATP into Galactose 1-phosphate + ADP + H
- Galactose 1-phosphate + UDP-GLC into Galactose Uridine Diposphate (UDP-GAL) + Glucose 1-phosphate
- Galactose Uridine Diphosphate into UDP-GLC
- UDP-GAL 4-epimerase
- Regenerates UDP-GLU
- UDP-GAL 4-epimerase
- Glucose 1-phosphate into Glucose 6-phosphate
Specifics:
Note that UDP-GLC is regeneratedLactase
Beta galactosidase of Lactose (GLU and GAL) disaccharide
Small IntestineLactose
Hydrolases
Specifics:
- Lactase activity normally declines to 5-10% of what it was at birth
LOC:
- Surface of intestinal cells
Terminology:
- Beta galactosidase - cleaves the beta bond between GLC and GAL
Diseases/Conditions:
- Lactose Intolerance/Hypolactasia
Lactose Intolerance
Lactose Intolerance/Hypolactasia
Deficiency in lactase
Carbohydrates - Lactose
ConditionsDiseases List
Fundamentals:
- Lactose is good energy source for intestinal flora
- Anaerobic fermenters
- Lactate is produced by these microorganisms
- Lactate draws water into the intestine as well as lactose
- Sufficient accumulation of water = diarrhea
- Lactate draws water into the intestine as well as lactose
- Severe accumulation hinders the absorption of other nutrients
Treatment:
- Avoid consumption of lactose
- Adding lactase to milk products
Glucose
Carbohydrates - Carbohydrate List
Cell Metabolism
Anabolism
Interlinking Pathways
Cell Metabolism
Ketose sugar
Funciton/Purpose
- Glucose is vital to certain organs that do not have the equipment to create glucose
Vital LOC:
- Brain - no gluconeogenesis but has mitochondria
- Skeletal muscle
- Red blood cells - no mitochondria
Glucose Metabolism:
CatabolismAnabolism
Interlinking Pathways
Conditions/Diseases:
Additional Information:
Conditions and Disease List
Medical Science
As it gets populated it will be further segregated into organ systems. It will be sweet, promise.
As it gets populated it will be further segregated into organ systems. It will be sweet, promise.
- Diabetes
- Wolman Disease
- Cholesterol Ester
- Cholera
- Necrotizing Fasciitis
- Whooping Cough
- Acute Myocardial Infarction (AMI)
- Lactose Intolerance
- Ethanol Sensitivity
- Hepatitis
- Galactosemia
- Cataracts
- Hers Disease
- Salivary Gland Infections
- Snake Venom
- Cystic Fibrosis
- Malaria
- Hemolytic Anemia
- I-Cell Disease
- Wernicke-Korsakoff Syndrome
- Respiratory Distress Sydrome
- Rickets
- Osteomalacia
- Caritine Deficiency
- Obesity
- Phenylketouria
- Muscle Wasting
- Severe Combined Immunodeficiency
- Gout
- Lesch-Nyhan
- Iron Overload and Infections
- Wilson's Disease
- Idiopathic Hemochromatosis
- Thalassemia
Additional Information:
] Temp: Conditions & Diseases
ConditionsDiseases List
ConDis
desc- Frequency
Fundamentals:
LOC:
Causes:
1)Genetic:
2)Pathogenic:
3)Biochemical:
4)Anatomical:
Route Of Transmission ROT:
Pathogenesis:
1)Genetic:
2)Pathogenic:
3)Biochemical:
4)Anatomical:
Symptoms:
Diagnosis:
Treatment:
Prevention:
Additional Information:
Diabetes
ConditionsDiseases List
Type 2: insulin resistance - insulin nondependent
- Two Main Types:
Type 2: insulin resistance - insulin nondependent
Causes:
?Genetic:
Route Of Transmission ROT:
LOC:
Pathogenesis:
Type 2- Insulin fails to inhibit the expression of a gene that encodes PEPCK and other genes of gluconeogenesis
- Increased output for glucose by the liver
- Without treatment type 2 may progress to type 1
Symptoms:
- Excessive thirst
- Frequent urination
- Blurred vision
- Fatigue
- Frequent/slow healing infections
- Hyperglycemia
Diagnosis:
Treatment:
- Weight loss
- Healthy diet
- Exercise
- Drug treatment
- enhance sensitivity to insulin
Prevention:
Additional Information:
Galactosemia
ConditionsDiseases List
- Disruption of galactose metabolism
- Deficiency in galactose 1-phosphate uridyl transferase activity
Causes:
Genetic:
Route Of Transmission ROT:
LOC:
Pathogenesis:
Symptoms:
- Vomit or diarrhea after consuming milk
- Hepatomegaly
- Jaundice
- Cirrhosis
- Cataracts
- Lethargy
- Retarded mental development
- Blood galactose elevated
- Galactose in urine
Diagnosis:
- Absence of transferase in red blood cells
Treatment:
- Remove galactose from the diet
- Prevents liver disease and cataract development
- BUT CNS malfunction/delayed acquisition of language skills
- Females = ovarian failurs
Prevention:
Additional Information:
Cataracts
ConditionsDiseases List
crystaline lens/anterior chamber becomes opaque decreasing vision
crystaline lens/anterior chamber becomes opaque decreasing vision
Fundamentals:
- Clouding of the normally clear lens of the eye
- If galactose 1-phosphate uridyl transferase is not active
- Aldose reductase converts Galactose into Galactitol
- Galactitol is osmotically active, water will difffuse into the lens forming cataracts
Causes:
- Aging process
- Trauma
- Glaucoma
- Medications
Genetic:
- Genetic
- Congenital anomaly Galactosemia
Route Of Transmission ROT:
LOC:
Pathogenesis:
Symptoms:
Diagnosis:
Treatment:
Prevention:
- Milk Moderation: NOTE THERE IS A HIGH INCIDENCE OF CATARAC
FORMATION WITH AGE POPULATIONS THAT CONSUME SUBSTANTIAL AMOUNTS OF MILK
INTO ADULTHOOD
- Too much of ANYTHING IS BAD theory
Additional Information:
Glycerol
Cell Metabolism
Glycerol Metabolism
Glycolytic and Gluconeogenic Pathway Glycolysis,Gluconeogenesis- Glycerol + ATP --> into Glycerol 3-phosphate ADP and H
- Glycerol Phospahte + NAD <--> Dihybroxyacetone Phosphate + NADH
- Dihydroxyacetone Phosphate (DHAP) <--> Glyceraldehyde 3-phosphate (GAP)
Additional Information:
Subscribe to:
Posts (Atom)