* what is the net gain / loss of ATP during: *
a) glycolysis?
b) TCA cycle?
c) cori cycle?
what is the net gain / loss of ATP during:
a) glycolysis: Net 2 ATP gain via susbtrate level phosphorylation
b) TCA cycle: Net 38 ATP gain via oxidative phosphorylation
c) cori cycle: Net 4 loss . Anaerobic
to make glucose, you need a source of energy and carbon units.
what are 3 sources of carbon that can be used in gluceoneogenesis?
what are 2 sources of energy that can be used in gluceoneogenesis?
what are the 3 steps of glycolysis that are metabolically irrervisble and need to be side stepped to in order to produce glucose in gluconeogenesis?
3 irreversible steps are in glycolysis:
enyzmes used to reverse ^^ reactions:
Acetyl co-A is a product of of fatty acid break down.
how do high levels of acetyl co-a influence gluconeogenesis?
high levels of Acetyl Co-A:
activates pyruvate carboxylase (used in step 1 of malate cycle: drives gluconeogenesis from pyruuvate -> PEP & eventually glucose)
inhibits: pyruvate dehydrogenase complex (prevents pyruvate being turned into acteyl co A & sparing it, leaving for gluconeogenesis)
the cori cycle spares pyruvate be ensuring that pyruvate is NOT converted to what?
where is a source of ^ instead?
the cori cycle only works if you conserve pyruvate, by removing it from muscle and recycling in the liver. cori cycle has to avoid pyruvate’s conversion to acetyl Co-A
INSTEAD
fatty acid metabolism produces acetyl co-A, creating another source of acetyl co-A & means that cori cycle can go ahead for gluconeogenesis. otherwise the pyrvate from cori cycle would be used to make actetly co-A . good thing !!
gluconeogensis from glycerol:
what is glycerol converted to? what does this get converted to?
where? (2)
Q
specifically, how is gluconeogensis controlled by:
(.i.e. which enzymes blocked etc)
explain how diabetes disrupts gluconeogensis pathway ox
insulin doesnt work:
SO
- pyruvate dehydrogenase remains phosphorylated & therefore inactive
- = less acetyl co-A to go into krebs cycle from pyruvate
- instead fats are broken down to produce fatty acids & acetyl co-A & goes into krebs cycle instead
- means that pyruvate is available for gluconeogenesis
which a.a are main glucogenic a.a? [2]
which a.a are ketogenic?
glucogenic amino acids: **alanine & gluatamine
lysine and leucine**
are ketogenic
which cells regulate water contents in the gut?
what is the mechanism of this?
secretory cells of the intestinal crpyts:
- CFTR channel within these cells controls this:
a) Cl- moves from ECF via Na/K/CL2 cotransporter (as does Na & K)
b) Cl- enters lumen through CFTR channel
c) Na+ is reabsorbed via Na/K ATPase
d) negative Cl- in lumen attracts Na by paracellular pathway (through cell gaps)
e) water follows the Na into the lumen

how does cholera effect the secretory cells of the crypts?
= secretory diarrhoea
Q
what is MoA for when ORS treats cholera?
ORS MoA:
what is hyperglycemia - why is it bad? explain the mechanism
hyperglycemia = high blood glucose
why bad?
= server water loss !
what can the following causes of oedema be caused by?


gastric epithelial cells
1. HCl is only produced when food is in the stomach = get unstimualted and stimulated parietal cells:
a) unstimulated parietal cells have H+ ATPase Pumps in the cytosol
b) stimulated parietal cells have H+ ATPase Pumps on apical surface
which cells produce gastrin?
when do cells produce gastrin?
where are they?
why is gastrin produced?
produced by: G cells !! g 4 gastrin xox
located @ atrium of stomach -> bc at the bottom of the stomach. if they sense that there are big proteins - stimulate the formation of more acid.
BUT HOW COMMUNICATE to the other cells?
what are 3 medical options for GORD?
why do u have to be careful if taking NSAIDS with GORD / GERD? (2)
how does Helicobacter pylori cause a peptic ulcer? (4)
which cells do you find in the body of stomach? [3]
which cells do you find in the antrum of stomach? [3]
which cells do you find in the body of stomach: parietal cells, chief cells, D cells
which cells do you find in the antrum of stomach: G cells, mucous cells, D cells
* MESS NOTES *
describe the differences of pH within the stomach and why they occur
cell surface = pH 7: HCO3- layer neutralises stomach acid = chemical barrier
then
mucous layer: physical barrier
then
stomach acid = pH 2
explain a) hormonal control of intestinal stage of stomach acid secretions xo
b) nervous control
Primarily inhibits gastric acid secretion when FOOD AND ACID ENTERS THE INTESTINES
NERVOUS CONTROL:
HORMONAL CONTROL:
How can you diagnose H. pylori presence? (4)
Acetyl Co-A is one of the starting molecules needed for TCA. But what is the equation for the formation of Acetyl Co-A from pyruvate?
what is the enzyme used to catalyse this reaction?
what nutrition is needed for this reaction?
- pyruvate + CoA + NAD+ –> acetyl Co-A + Co2 + NADH