6.1 Acid/Base balance Flashcards
normal range of urine pH
4.5-8.5
Explain how alkaleamia leads to numbness/tingling/muscle twitches
-promotes COOH to COO- on albumin
-more Ca2+ binds to albumin
-less free Ca2+ in plasma, so can’t stabilise myocardium VGNaChannels
-increased neuronal excitability, so APs fire with less stimulus
explain how acidemia leads to arrhythmias
-promotes COO- to COOH on albumin as H+ binds to try and reduce pH
-less Ca2+ bound to albumin
-more free calcium in plasma
-also increases plasma K+ conc, affects excitability of cardiac muscles so difficult to depolarise and cause an AP
what is meant by HPO42+ being a tithable buffer?
can form a weak acid when bound to H+
how is NH4+ in lumen a buffer of pH?
keeps H+ bound, and can’t diffuse readily so H+ ‘locked up’
link between acidosis and hyperkalaemia
CD increases K+ reabsorption so H+ can be taken out of blood
also other way round, if too much K+ in blood then H+ brought out of cells to take K+ in
link between alkalosis and hypokalaemia
CD decreases potassium reabsorption and so more H+ goes into blood
renal compensation respiratory alkalosis
-less HCO3- reabsorption from PCT
-HCO3- secreted from last DCT/CD
-H+ reabsorbed with K+ from last DCT/CD
causes of metabolic acidosis
lactic acidosis
ketacidosis
diarrhoea (loss of HCO3-)
what is the anion gap? what’s measured?
difference between measured cations and anions?
na, k - cl, hco3
when is the anion gap increased?
if HCO3- replaced by other anions (not measured ones) e.g. DKA, aerobic respiration
when is anion gap unchanged?
renal causes of acidosis as HCO3- deficiency replaced by Cl-
causes of hypokalaemia
-vomiting
-renal loss: diuretics, excess aldosterone, renal tubular acidosis
-alkalosis
how does renal tubular acidosis cause hypokalaemia?
not eliminated H+ so lose K+ to balance out
