CMB Exam 2 - Details Flashcards
Lewis acid
e- acceptor (ie any ion/molecule that can accept a pair of nonbonding valence electrons). eg CO2
Why/how is there such a big discrepancy between H+ and HCO3- levels?
We need the excess HCO3- buffer for pH and to accomodate the continuous production of organic acids. Discrepancy established by kidney actively excreting H+ and actively reabsorbing HCO3-.
How does the body monitor blood pH?
Chemoreceptors in the carotid are sensitive to pO2, pCO2 and/or pH
respiratory compensation
In the case of acidosis, resp. rate increases to breathe off more CO2. In the case of alkalosis, resp. rate decreases.
anion gap
~12 ± 4 mEq/L = the quantity of anions in the serum (mostly HCO3- and Cl-) not balanced by cations (mostly Na+). Plasma is electro-neutral, so the “gap” of is actually balanced by negatively charged proteins. Exogenous acid increases the gap.
Derive the equation for the pH of blood.


What is normal arterial [HCO3-]?
~24 mEq/L HCO3-
What is normal arterial pCO2?
~35-45 mmHg CO2
Why is fructose more “evil” than glucose?
In the liver, since it can’t enter PP pathway or glycogen synthesis it’s preferentially converted to F1P to FA to TG to VLDL, bypassing glucokinase and PFK-1 (which are important regulators). This can also lead to deficiencies in aldolase B, causeing accumulation of F1P. Can rapidly deplete liver ATP/Pi levels and increase uric acid production (gout, hypertension).
normal fasting glucose levels
80-140 mg/dL (centered around 110 mg/dL)
Which enzymes are activated by glucagon? What are the results of this change?
Activation of: PKA, F-2,6 bisphoshatase, phosphorylase kinase, glycoden phosphorylase, hormone-sensitive lipase. This results in activation of gluconeogenesis and glycogenolysis.
Which enzymes’ activity is inhibited by glucagon? What are the results of the changes?
Inhibition of: PFK-2, PFK-1 indirectly, pyruvate kinase, glycogen synthase. Results in inhibition of glycolysis and glycogen synthesis.
What are the major gluconeogenic substrates?
Lactate, glycerol, and amino acids (except leu and lys). NEVER acetyl-CoA fatty acids.
“limit dextrin”
Glycogen with the 4-residue branch
acid maltase
Degrades glycogen in the lysosomes.
What are the three main categories of glycogen storage diseases?
Hepatic, myopathic, or “miscellaneous”.
How can insulin resistance directly increase blood glucose?
Lower insulin sensitivity causes lipolysis and increases fatty acid oxidation, which will decrease glucose utilization in the muscle and increase gluconeogenesis in the liver.
adiponectin
Activates AMPK, which appears to enhance insulin sensitivity; is anti-inflammatory; improves clearance of FFA, glucose and TG; suppresses gluconeogenesis
AMPK
Activated says LIVER: Increases glycolysis and decreases gluconeogenesis in the liver; MUSCLE: increasing FFA uptake, β-oxidation, and glucose uptake in the muscle.
What happens to glucagon levels as DM-2 progresses?
Glucagon response decreases as DM-2 progresses (meaning that instead of responding, it stays high).
Why can’t glucometers be used in diagnostics for glucose disregulation?
Glucometers have high variability at high glucose levels, so they are NEVER used for diagnosis
When can a random blood glucose test be diagnostic for diabetes?
When it’s over 200mg/dL AND the patient shows Si/Sx.
HbA1C
Diagnostic for diabetes when >6.5%
isomers
Two molecules with the same chemical formula but different arrangement of bonds/atoms.