Session 6 Flashcards
(58 cards)
A change in one pH unit represents a
10 fold change in H+ conc
PH of the urine varies between
4.5 and 8.4 depending on the bodies need to excrete H+ or HCO3-
What is the consequence of alkalemia on free calcium
Lowers free calcium by causing Ca2+ ions to come out of solution
Alkalemia = not enough H+, H+ dissociated from COOH on albumin, therefore COO- negative site for Ca2+ to bind
Consequence of lowering free calcium
Increases neuronal excitability
Fire action potentials at slightest signal
Numbness or tingling
Muscle twitches
if severe- sustained contraction (tetany) that paralyse respiratory muscles
Acidemia impact on free calcium
Increases free calcium by causing Ca2+ ions to go into solution
Acidemia= increased H+ in blood, binds to COO- on albumin, decreased negative sites for Ca2+ to bind to, more free in blood
What other impacts does Acidemia have apart from increasing free calcium
Increases plasma potassium ion concentration due to K+ H+ exchange
-Affects excitability especially in cardiac muscles- arrhythmia
Increasing H+ denatured proteins
Sources of H+
Diet, metabolism (breaking down ketones, lactic acid…)
Normal plasma pH
7.35-7.45
Buffers in body
ECF = HCO3-
Cells = proteins, Haemoglobin, phosphates
Urine = phosphates and ammonia
H+ output
Ventilation, renal
3 mechanisms to control pH of blood
Buffers, ventilation, renal regulation of H+ and HCO3-
Time frames of pH homeostasis
Renal regulation is slower than buffers and ventilation (1-2 days)
2 ways in which kidneys alter pH
Directly, by excreting or reabsorbing H+
Indirectly, by changing the rate at which HCO3- is reabsorbed or excreted
pH management at proximal tubule
Carbonic anhydrase converts H+ and HCO3- to H20 and C02, which goes into cell and is converted back to H+ and HCO3-
H+ transported into lumen with Na+ exchanger, HCO3- transported into blood with Na+ cotransporter
PH drop stimulated glutamine to break down into 2 alpha KG and then 2HCO3-, which is transported into blood, and 2NH4+ which is broken down into NH3 and diffuses into lumen to bind to H+ and form NH4+
PH control at Late DCT/CD
K+ and H+ exchanged
Acidosis can cause
Hyperkalaemia, due to XS K+ reabsorption at CD so H+ can be taken out of blood
Hyperkalaemia can cause
Acidosis
Alkalosis can cause
Hypokalaemia, Decreased K+ reabsorption in CD
More pumped into cells, less absorbed into blood, so H+ can be absorbed into blood
Hypokalaemia can cuase
Alkalosis
Respiratory acidosis occurs when
Alveolar hypoventilation results in CO2 retention and elevated pCO2
More CO2 is combined with H20 and converted into H+ and HCO3-
Any compensation must come from renal mechanisms that secrete H+ and reabsorb HCO3-
What is more common respiratory alkalosis or acidosis
Alkalosis
Respiratory alkalosis is often a result of
Hyperventilation, alveolar ventilation increases without a matching increase in metabolic CO2 production
CO2 levels fall causing levels of H+ to fall
Primary cause is excessive artificial ventilation e.g. panic attack
Compensation for respiratory alkalosis
Any compensation must come from renal mechanisms
HCO3- not reabsorbed in proximal tubule
Late DCT/CD: HCO3- secreted, H+ reabsorbed with potassium
Metabolic acidosis occurs when
Dietary and metabolic input of H+ exceeds H+ excretion (lactic acidosis, ketoacidosis)
Can also occur if body loses HCO3- (diarrhoea)
