Acid-base balance Flashcards by Irene Xiao

define pH:

-ve log of H+ conc (mol/L)

pH = -log [H+]

[H+] = 10 ^ -pH

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normal ECF values:

~7.4
cell values at 7.2
(60 nM)

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arterial blood pH:

7.4

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venous blood pH:

7.36

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normal arterial pH maintained btw:

7.35 - 7.45

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acidotic and fatal pH:

<7.35 acidotic

<6.8 is fatal

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alkalotic and fatal pH:

> 7.45 alkalotic

>8 is fatal

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reactions increasing net body acid: list (5)

aerobic metabolism of carbs, fats, neutral aa to
sulphur w aa
aa w cationic side groups
phospholipids, phosphorylated proteins
incomplete metabolism of carbs during anaerobic exercise

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reactions increasing net body acid: aerobic metabolism of carbs, fats, neutral aa to produce-

CO2 in CAC

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reactions increasing net body acid: sulphur w aa produce-

produced H2SO4

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reactions increasing net body acid: aa w cationic side groups produce-

produce urea and H+

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reactions increasing net body acid: phospholipids, phosphorylated proteins produce-

H2PO4-

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reactions increasing net body acid: incomplete metabolism of carbs during anaerobic exercise produce-

produce lactate and H+

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major fuel source in diabetics:

fats for ATP prod
acetoacetic acid, ß-hydroxybutyric acid (ketoacids aka ketone bodies) also produced
true in starvation

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reactions increase net body base: list (2)

breakdown aa w anionic side groups

- metabolism of organic anions (eg. citrate, ascorbate)

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reactions increase net body base: breakdown aa w anionic side groups produce-

consumes H+

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reactions increase net body base: metabolism of organic anions (eg. citrate, ascorbate) produce-

produces HCO3-

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base/acid excess: diet rich in meat/protein vs. vegetarian

protein: excess acid (non-carbonate, non-volatile)
veggie: slight base excess

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loss of: vomiting

loss of HCl (acid)

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loss of: diarrhoea

loss of NaHCO3 (base)

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pH homeostasis: maintained by list (3) and time taken

immediate neutralisation of added base/acid by buffers (secs)
continuous controlled removal of CO2 by lungs (mins)
maintenance of ECF [HCO3-] by kidneys (hrs to days)

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pH homeostasis: long term features

homeostatic control of ECF pH requires balancing endogenous (from aerobic respiration)
exogenous (food) input of acid and base w their output from body
instantaneous pH regulation vital
physiological processes take time
chemical buffering is interim measure to ensure pH remains in narrow range

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buffering: acids defined as

H+ donors

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buffering: bases defined as

H+ acceptors

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conjugate acid base equation:

acid base + H+

buffering: what acts as pH buffers

conjugate acid/base pairs of weak acids

acid dissociation constant (equilibrium constant) equation

Ka= [base] x [H+] ÷ [acid]

ECF buffers: list (3)

- HCO3-/ CO2 - proteins esp haemoglobin, albumin - H2PO4-/ HPO42-

which buffer accounts for 90% of ECF's buffering capacity btw pH 7.2-7.6

HCO3-/ CO2

ECF buffers: haemoglobin sig

- next most important after HCO3-/ CO2 - histidine residues act as buffers in haemoglobin - 36 in each haemoglobin - buffers btw pKa values of 6.5 - haemoglobin buffers acid derived from CO2 - therefore CO2 produced by cellular metab buffered by haemoglobin while being transported by blood to lungs for excretion

bicarbonate buffering sys: what is buffered in this sys

H+ from non-carbonate acids

bicarbonate buffering sys: equation

H2O + CO2 H2CO3 HCO3- + H+

bicarbonate buffering sys: HCO3-/ CO2 sys highly effective coz (2)

- conc of HCO3- in plasma is high (24mM) | - operates as regulated open sys, kidney controlling [HCO3-] and respiratory sys controlling plasmaCO2

controlled removal of CO2:

- by respiratory sys | - within body pCO2 controlled by resp sys in response to arterial (eventually CSF) pH

pH stabilisation in body: continued input of acid

- HCO3- continually consumes to buffer non-carbonic acids

pH stabilisation in body: role of kidney list (3)

- HCO3- filtered into kidney tubules reabsorbed, not lost to body - additional HCO3- molecules created by kidney tubule cells, transported into plasma to replenish alkaline store - non-carbonate acids r excreted

pH stabilisation in body: to increase body HCO3- lvls

- organic anions (bases) added to body r metabolised to HCO3-

pH stabilisation in body: excess HCO3- removed by

- allowing appropriate amount of HCO3- filtered into kidney tubule to be excreted

reabsorption of filtered HCO3-: conc of HCO3- higher in plasma or ECF?

plasma | - 24mM

reabsorption of filtered HCO3-: how much filtered HCO3- reabsorbed?

almost completely

reabsorption of filtered HCO3-: depends on? and locations

- from tubular fluid active transport of H+ into tubular fluid - LUMINAL Na/H antiport in proximal tubule and luminal H+ pump in collecting duct

reabsorption of filtered HCO3-: most of reabsorption occurs in

proximal tubule

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: how is H+ transported into lumen

- actively transported | - bound by basic form of non-carbonate buffers (mainly HPO4 2-)

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: HCO3- generated in cell?

- to produce H+ for export = net increase in HCO3- | - 'new' HCO3- ion transported into blood

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: HCO3- reabsorption, location

- tranporter on LUMINAL membrane - Na/H antiport in proximal tubule - also proton pump in collecting duct

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: luminal Na/H antiport only secrete at?

- against modest pH grad so tubular fluid (proximal tubule) not fall below 6.8

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: H+ pump can produce tubular fluid pH low as, where?

4.5 in collecting duct

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: titratable acids have pKa values btw, sig?

- 4.5-7.4 (pH of glomerular filtrate) | - effective buffers at pH of urine

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: list titratable acids (4) and key

- urate - creatine - beta-hydroxybutarate - HPO4 2- will bind to H+ in tubular fluid

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: pKa- urate

5.8

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: pKa- creatine

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: pKa- betahydroxybutarate

4.8

excretion of titratable (non-carbonic) acid/ HCO3- regeneration: pKa- HPO4 2-

6.8

excretion of ammonium (NH4+)/ HCO3- regeneration: glutamine features

- made from liver, mm and gut - taken up from blood into proximal tubule - neutral aa w 2 nitrogenous side groups

excretion of ammonium (NH4+)/ HCO3- regeneration: glutamine converted into

- å ketoglutarate (AKG2-) w 2x NH4+ produced -> glucose (will consume a H+ in this step)

excretion of ammonium (NH4+)/ HCO3- regeneration: glutamine products excreted

- NH4+ ions excreted in urine | - 2x HCO3- (which provided H+ ends up in blood)

excretion of ammonium (NH4+)/ HCO3- regeneration: sig of excreting NH4+

- or will be converted into urea in liver= releasing 2x H+ cancelling out HCO3- gained by ECF

excretion of ammonium (NH4+)/ HCO3- regeneration: NH4+ is it titratable? and pKa

- NH4+ not titratable acid, v weak acid | - pKa= 9

regulation of kidney function: how

- active secretion of H+ into tubular fluid - drives HCO3- reabsorption and regeneration is increased by sys acidosis - glutamine uptake by tubular cells increased at acidic pH

control of cell pH: how does cells maintain pH ~7.2 despite acid producing metabolic processes? list (3)

- rapid efflux of CO2, end product of ox phos - intracellular buffering mainly by HCO3-, cellular proteins, organic phosphates (eg. ATP), lesser extent: inorganic phosphates (H2PO4-/ HPO4 2-) - exporting H+ via H/Na exchanger

summary: (3)

- resp sys reg so daily CO2 prod excreted in expired air (lungs), constant pCO2 is maintained - H+ liberated from non-carbonic acids instantly buffered, eventually by HCO3- - HCO3- used up replaced in kidney - kidney also excretes some acids such as H2PO4- - resp and renal sys both maintain body pH by holding ratio of [HCO3-]/[CO2] constant rate

Acid-base balance Flashcards

(61 cards)