anatomy pics of arteries. incomplete but i think this is what u guys want?

physio respiratory mini control

questions:
1. blood oxigen capacity
2. content of air in atmostphere
3. purpose of ventilation
4. content of alveoli gas
5. draw oxigen-haemoglobin saturation disassociation graph
6. diff forms of transport of CO2 and O2 in blood
7. func of carbonic anhydrase
8. partial pressure of O2 in our cells

my answers:
1. 10-20ml per 100ml blood
2. O2 : CO2 : N2 : H2O :: 20.87% : 0.03% : 78.6 : 0.5
3. no idea, figure out urself >,<"! just crap something lar.
4. O2 : CO2 : N2 : H2O :: 13.5% : 5.3% : 74.9% : 6.3%
5. uhm, its the bloody sigmoid thing.. saturation % vs oxigen pressure graph
curve goes left if temp down, presure down, ph up.
curve goes right if temp up, pressure up, ph down
6. transport of O2
1.5% in plasma
98.5% in hb-o2 [ in rbc]

transport of Co2
7% in plasma
23% in hb-co2 [in rbc]
70% in form of HCO3

7. function of carbonic anhydrase
IN RBC, it catalyses the binding of H2O with CO2 and forms H2CO3.
H2CO3 is then converted into HCO3.
HCO3 then goes into the venous blood.
H+ from H2CO3 goes to dispose other Hb-O2 and makes it Hb-H. The O2 goes into the tissues.

8. according to lecture it is
Po2 = 10
Pco2 = 60

according to my reference it is
Po2 = 40
Pco2 = 45

bie bie ..gluck

reference for answers are mostly lecture of last week.

biochem tasks control 3, carbohydrate

so, until now i only managed to create this..

2. White muscles usually only perform aerobic glycolysis because postural maintainance movements hardly leads muscle to exhaustion. In addition to that, white muscles has a high fatique rate. In general, skeletal muscles are able to perform glycolysis even during anaerobic conditions. However the end product would be lactate. Why lactate? Due to the production of NADH2 during the 6th glyceraldehyde dehydrogenase reaction.Then it requires a place for NADH2 to be oxidised. In a normal senario we are able to send the NADH2 into respirative phosphorylation chain for oxidation. However, in anaerobic situation it is not possible. Thus, the lactate dehydrogenase[LDH] oxidises the NADH2 at reaction 11 of glycolysis.

inhibition of LDH would then result accumulation of NADH2. which probably will allosterically inhibit enzyme 6.

3.

4. glycogen phosphorylase of skeletal muscles has higher Vmax due to the requirement to induce a huge amount of glucose-6-phosphate release at the spur of the moment that muscle action is needed. The glycogen phosphorylase of liver has alot of time to slowly release glucose because there is no real dire need for glucose, it is just to maintain the body's blood glucose rate.

5. not very possible due to no ATP production from those processes.

6. treat bicarbonate as the CO2 that is required for the 1st reaction of pyruvate decarboxylase.

7.From the view of glycolysis:

A rising ATP conc means that AMP is yet to be present to activate PFK I complex. However, ATP will be used by PFK 2 to catalyse fructose2,6-bisphosphate. The F2,6-bp will then allosterically activate PFK 1 and change its conformation into a conformation rather similar if the AMP activates it. Now, why do AMP is the activator of PFK 1? This is due to AMP is the signal of used ATP, which is followed by the excessive usage of ATP in muscles, which in turn signify that muscle has been put to much work. Thus, F 2,6-biphos will help the degeneration of glycogen to provide glucose.

a rising AMP conc will allosterically activate PFK 1 complex.

From the view of gluconeogenesis:

ATP increase will activate gluconeogenesis and AMP increase will activate glycolysis

8.

10. 2 NADH2 molecules are formed. In the case of aerobic condition, NADH2 = 3 ATP. Thus 6 ATP is generated and outweights the ATP used in glucokinase and phosphofructokinase reactions. Net ATP = 4.

11. through oxidative phosphorylation pathway 3 ATP is generated of each NADH2. So 2 NADH2 will generate 6 ATP and the net ATP gain is 4 ATP.

12. Synthesis of glucose will increase due to

13.

14. could this substance be protein kinase c???

15.

16. This procedure saves the 1 ATP that is used by hexokinase aka glucokinase to add the phosphate back to glucose that results the formation of glucose 6- phosphate. This process is only possible due to sm glycolysis is used up at the time of release. Thus, saving the 1 single ATP does not affect the blood glucose levels unlike in liver.

17. glucose lvl blood drop , glycolysis drop, glycogen decomp drop, glycogen synthesis up.

18.

19.

1. Myocardium infaction = no oxygen. This results the anaerobic affinity of LDH to work [LDH4,5 which is at muscles]

2. Acute hepatitis = ???

20. glucose levels will go up due to glycolysis. Glycolysis by epineprine is possible to be activated by 2 receptors which have their own diff pathways.

1. Receptor alpha does the PIP2 CA2+ signal transduction method. [which ultilizes IP3 DAG + calcimodulin,it is an intracellular receptor pathway]

2. Receptor beta does the typical glucagon pathway. Which is cAMP signal transduction method [ intracellular, which requires adenylate cyclase]

21. insulin. For which test, maybe check ur biochem workbook.

22. its all about PFK 1. The increase in AMP due to continuous usage will result allosteric activation at PFK 1. [ATP]/[AMP] ratio will also decrease and the less ATP is a signal for PFK 2 to convert fructose 6 phosphate into fructose 2,6 phosphate that binds to the simillar purine allosteric site at PFK 1 and creates a change in conformation that resembles the allosteric activation of PFK1. In both bindings, rate of PFK 1 converting fructose 6 phosphate to glucose 2,6-phosphate with the usage of 1 ATP results in speeding up the glycolysis.

23.