Deoxyhemoglobin has a higher pKa than oxyhemaglobin and thus will accept hydrogen ions more readily. This is important in the ability to "carry" CO2 as the main mechanism of CO2 transport is actually conversion of CO2 to HCO3- (CO2 + H2O -> HCO3- + H+), thus deoxyhemaglobin carries the H+ while HCO3- is transported in the plasma to the lungs. Carbaminohemaglobin is actually only about 20% of the CO2 trasnport and CO2 dissolved as CO2 is 10%; trasnport as HCO3- is around 70% of the CO2 transport.

Here is another image of the process.

Another important aspect of the process to take note of that they like to ask about is the chloride shift. Chloride moves the opposite direction as HCO3- in the RBC. Thus at tissues where we are generating HCO3- from CO2 and need to pump it out of the cell, chloride moves into the cell.At the alveoli where we need to pump HCO3- back into the RBC to turn it into CO2, chloride moves out of the cell.

Other answers:

• 2,3BPG will bind and stabilizes deoxyhemaglobin making it less attracted to oxygen, shifting the hemaglobin dissosiation curve right.
• Deoxyhemaglobin has a higher capacity to form carbanimohemaglobin
• Deoxyhemaglobin has a higher pKA than oxyhemaglobin (this is why it can accept hydrogen ions more readily)
• Competition for binding site is not a major mechanism for the ability to carry CO2 as most CO2 is "carried" by conversion to HCO3-
• Nitric oxide binding is not a mechanism of CO2 carry.

First question : They tell us its a lymphocytic leukemia

Second question : Deciphering whether it is a B cell or T cell.

The cells have no surface bound Ig M ,Ig G or cytoplasmic chains for these antibodies , but have a rearranged gene segment( meaning active ) for the T cell Receptor . So the Cells are T Cells

Third question : Now that we know that they are T Cells , we want to know whether they are CD4 or CD 8 positive

The cells in the clinical vignette lack both CD4 and CD 8 ( double negative ) According to how T cells normally develop - They start of as being double negative ( i.e not expressing CD4 or CD 8) in the subcapsular region and progressively become
- positive for both CD 4 and CD 8 in the cortex
- and eventually acquire the TCR and CD3 by the time they get to the medulla

These cells therefore must T lymphocyte thymocytes localised to the cortex

Here is my take: a ventricular septal defect in infancy allows for left to right shunting of blood in the ventricles. This causes an increased pressure in the right ventricle (due to more blood being pushed into it) and a decreased pressure in the left ventricle. Because there is more blood in the pulmonary circulation from the shunt, I think the left atrial pressure would also be increased in an early VSD.

SO when you repair the VSD, the left ventricle pressure will be increased compared to when the shunt was present (it is no longer losing blood), the right ventricle pressure will be decreased (it is no longer getting blood from the shunt), and the left atrial pressure will be decreased (there is no longer overload of the pulmonary system returning to the left atrium).

FA2020 p298

Here, we want to know loading dose which is equal to the volume of distribution x target concentration in plasma.

So our loading dose = 1.81L/kg x 10mg = 18.1mg/kg

She is a 55kg person so 18.1mg/kg x 55kg = 995.5 mg which approximates to 1000mg total loading dose.

Important Pharm Equations to Remember