Acids, Bases, and Buffers Flashcards
Law of mass action
A + B –> C + D
Vf= kf[A][B]
Vr=kr[C][D]
keq= products/ reactants
Keq
Keq = kf/kr = [C][D]/ [A][B]
Products/reactants.
Measures position of the equilibrum.
Acid
Likes to give away protons
pH of ECF
7.4
pH of ICF
6.9
Neutral solution
[H+]=[OH-]
ph=pOH=7
Arterial and Venous blood pH
Gastric juice
Arterial: 7.34-7.44
Venous: 7.28-7.42
gastric: 1.4-3.0
Equilibrium between acid and its conjugate base in aqueuous sol’n
HA + H20 –> H30+ + A-
HA –> H+ + A-
Strong vs weak acids/bases
Strong are completely dissociated in water, weak are reversibly protonated/deprotonated
pKa
How strong is your acid/base?
Measure of how much you like to give away/accept protons
low pka= strong acid. High pka= strong base.
pka= -log10Ka
Henderson-Hasselbach
ph= pka + log([proton acceptor]/[proton donor])
[A-]/[HA]
or ph = pka + log([acid]/[base])
Medically important weak acids
H2Co3
H2Po4
Histidine is important regulator of pH (often is changed)
Diabetics, acetoacedic acid.
Medically important weak bases
Purines, pyrimidines
Amphetamines, AZT, loca anesthetics.
Lidocaine
weak base. In more alkaline ECF it is uncharged and freely diffuse, and when it gets to more acidic ICF it gets protonated and charged so it’s trapped in ICF and can have effects.
Bacteria in the stomach
How does it survive low ph? it creates local enviro that is neutral pH. Produces urease to change urea to bicarb and ammonia ions (neutralizes HCl acid locally on surface of mucosa and bacteria can live).
Aspirin
Take aspirin with pka 3.5, at low pH predominantly protonated and gets absorbed.. lower down in duodenum where pH is higher aspirin is in dissociated neg charged state and is absorbed by a diff. mechanism (antacids can raise pH of stomach and affect drug absorption of weak acids/bases)
ph= pka when?
The acid or base is 50% dissociated and conc of A- =HA
AH + B –> A- +BH+
AH is acid, A- is conjugate base
BH+ is conjucate acid
Ka
Ka = (h30+)(A-)/ (AH)
AH + H20 –> A- + H30=
ph
Ph= pka - log (AH/ A-)
ph > pka
acid exists as A- in H2-, and is fairly soluble
ph < pka
acid is HA is water and is LESS soluble. (vice versa for a base).
Titration Curve
Effective buffering occurs in range from [A-] / [HA] = 0.1 to 10 or w/in 1 ph on either side of Pka
Henderson-hasselbach determines shape of this. when ph=pka slope flattens (don’t get large effect on changing conc of bicarb or Co2)
When pH changes by 0.3 units
The H ion concentration doubles from 40 to 80
Respiratory acidosis
High pC02 (have increased Co2, compensate by increasing Hco3- absorption).
Buffer
A mixture of weak acid HA and its conjugate base A-
Bicarbonate buffer system
H+ + HCO3- –> H2Co3 –> H20 + CO2 (d) –> Co2 (g)
First parts are aqueous phase in blood, last is air phase in lung.
Open system. Conc of carbonic acid determined by amount of CO2 dissolved in blood (regulated by breathing).
Co2 regulated at other end by selective retention/secretion of bicarbonate by the kidney.
Memorize Normal Concentrations
pCo2= 40mmHg
[HCO3-] = 24mM
[CO2]= 1.2 mM
Blood pH = 7.4
Kidney and lung regulate this (kidney excretes H/Hco3-)
Memorize this equation
pH= 6.1 + log[HCO3-] / 0.3*PCo2
Normal: ph = 6.1 + log24/0.3*40
ph= 7.4
Effect of Co2 levels
High levels Co2, make more acidic, respiratory acidosis
Low levels of CO2 more basic, respiratory alkalosis.
Effect of carbonic acid levels
Low carbonic acid level, lower pH, metabolic alkalosis
High carbonic acid levels, metabolic acidosis.
