pH Flashcards
what does pH depend on?
pH depends on the
ratio of [HCO3-] to pCO2
what is the normal range of plasma pH ?
if pH is below this range then it is called?
if pH is above this range then it is called?
7.35 – 7.45
which is a concentration of between 44.5 and 35.5 nmol/L of H+ ions
- below this range, condition is known as acidaemia.
- above this range, condition is known as alkalaemia.
how do the kidneys and lungs work together to control plasma pH ?
Kidneys
• Control pH – variable recovery of hydrogen carbonate and active secretion of hydrogen ions
Lungs
- Alveolar ventilation allows diffusion of O2 into blood and CO2 out of blood – control pO2 and pCO2
- Rate of ventilation controlled by chemoreceptors
effect of alkalemia on Ca+
in alkalosis, there is less H+ available, so the albumin is left with COO- ends,
this attracts Ca+ to leave their solution and binds to it, therefore u get less free Ca+ available!
HYPOCALCEMIA
effects of hypocalcemia
normally resting state of Na+ ions is stabilized by Ca+ ions (preveting free spontaneous depolarization)
paresthesia and tetany
If the pH rises above ______, 45% of patients die
7.55
why does acidaemia cause hyperkalemia?
why is this dangerous?
to compensate for the high levels of acid H+ in the blood,
cells EXCHANGE their K+ with H+, causing high K in blood!
high K+>> arrythemias!
what can increasing H+ ions cause?
can effect enzymes>> binds to proteins & denatures proteins!
this effeects muscle contractility, gylcolysis, hepatic functions!
In acidemia, since the H+ ion concentration in ECF is so low, if we add very small amounts of acid this would change the concentration & pH dramatically.
but this is not the case in our body….why?
bc H+ ions are buffered by binding to various sites.
In acidosis, how is pCO2 is lowered?
what pH does acidosis become fatal?
by increasing ventilation
below 7.0
what is the most important ECF buffer?
The most important ECF buffer is the
CO2/HCO3-
Describe the CO2/ HCO3 buffer system
determined by?
controlled by?
disturbed bh?
how do H+ ions that r produced metabolically, effect the concentration of HCO3-
If H+ ions are produced metabolically ,
they react with HCO3- to produce CO2 in venous blood,
which is then breathed out through the lungs,
leaving a directly proportional deficit of [HCO3-] in arterial blood :(
in alkalosis, when pCO2 may be slightly raised, why is compensation limited?
compensation is limited by hypoxia resulting from hypoventilation.
what does correction of the acidosis or alkalosis depends upon?
the kidney variably excreting or creating HCO3-.
Describe the cellular mechanisms for reabsorption of HCO3- in the proximal tubule of the nephron
Na-K pump, when NA is pumped out> NA inside the cell is LOW> this creates a gradient where Na+ from lumen can now come in!
THIS IS WHAT DRIVES the Na+-H+ exchanger!
ok…moving on to HCO3-….
it is filtered in considerable quantities at the glomerulus – about 180 mmol/hour.
recovering HCO3- on it own isnt enough cuz weyre using it all up in metabolism due to producing acid!!
so reabsorption of all filtered HCO3- is still not enough to restore plasma HCO3-!
SHIIIIIITTT
so HCO3- will have to be created within the kidney.
where is final site for HCO3- absorption and H+ excretion.
what type of cell does this occur in?
Describe the cellular processes
H+ buffered by ammonia and phosphate (‘titratable’)>> bc we dont want our tubules to be too acidic
– Produce NH4+ and H2PO4- which are excreted
A -intercalated cell
how do we produce acid?
how come this does not deplete HCO3-
Normally we produce acid due to metabolism (breakdown if proteins)
This does not deplete HCO3- because:
– The kidneys recover all filtered HCO3-
– Proximal tubule makes HCO3- from amino acids, putting NH4+ into urine
– Distal tubule makes HCO3- from CO2 and H2O; the H+ is buffered by phosphate and ammonia in the urine
How does the kidney make new HCO3-?
where in the kidney does this happen?
PROXIMAL
Break down of a.a> glutamine (Glut):
- alpha-ketoglutorate yields>> 2 HCO3-, which enters the blood , (in effect, this is indirect excretion of H+ attached to ammonia).
- Ammonium is made & dissocites into ammonia and free H+ ions (this must happen cuz we cant have free H+ ions in the blood)
the ammonia ions can cross the membrane & into the lumen & bind to free H+ ions to form AMMONIUM!> IS CHARGED AND TRAPPED IN THE LUMEN!
This process takes place largely in the proximal tubule, but is supplemented distally.
Describe the mechanism of buffering H+ in the urine and explain the concept of titratable acid and the role of NH4+
- free H+ r like little snakes that bite anyone if not captured!*
- so we need to cage them!*
so most of the excreted H+ reacts with buffers and remains in the urine.
One such buffer – monobasic phosphate (HpO-4) becomes more effective as the pH of urine falls (acidic).
ALSO, H+ can bind to ammonia ions in the lumen to make>> AMMONIUM!>>we pee it out!
Describe the Renal Responses to Respiratory acidaemia (acidosis)
u get a fall in renal tubular pH bc of the diffusion of extra CO2 into the cells > leads to increased excretion of H+> with more production and reabsoption of HCO3-,
restoring the ratio of HCO3- to pCO2 nearer to normal
so remember for each H+ secreted, a HCO3- is reabsorbed!
Describe the Renal Responses to Respiratory alkalaemia (alkalosis):
what is the anion gap?
how do u calculate it?
The value normally ranges from 8-14 mmol/L and
the reason for this difference is bc not all the anions r measured, there r also other things with negative charges (anions) present (ex: protiens)
Difference between measured cations and anions
([Na+] + K+]) – ([Cl-] + [HCO3-])
exaplain the effects on the kidney if excess acid is produced .
what would happen to the anion gap?
if excess acid is produced, the associated anion (e.g. Lactate) will replace HCO3- in plasma, which will influence the anion-gap.
If HCO3- is replaced by another anion which is not included in the calculation >> the gap will increase.
common causes of metabolic alkalosis,
• In metabolic alkalosis HCO3- is retained in place of Cl-
• Stomach is a major site of HCO3- production
– Severe prolonged vomiting - loss of H+
– Or mechanical drainage of stomach
what if u get metabolic Alkalosis & volume depletion?
why would compensating be difficult in this stage?
in order to maintian blood V. the Na-H exchanger would still keep working (in order to try to reabsorb more Na)
- this will make it difficult to lose the HCO3-,*
- bc it keeps getting reabsorbed!*
common causes of metabolic Acidosis w/ increased anion gap
If anion gap is INCREASED – indicates a metabolic production of an acid
– Keto-acidosis
• diabetes
– Lactic acidosis
• Exercising to exhaustion
• Poor tissue perfusion
– Uraemic acidosis
• Advanced renal failure – reduced acid secretion, build up of phosphate, sulphate, urate in blood
how does DKA cause metabolic Acidosis?
the H iions then use up the HCO3- and uve got ketones left instead of the HCO3- and theyre acting as the anions!
and therefore theyre not measured.
so u get an increase in the anion gap!
conditions that lead to respiratory Acidosis?
• Type 2 respiratory failure
– Low pO2 and High pCO2
– The alveoli cannot be properly ventilated
– Severe COPD, severe asthma, drug overdose, neuromuscular disease
conditions that leads to respiratory Alkalosis?
• Hyperventilation
– Anxiety / panic attacks – acute setting – Low pCO2, rise in pH
• Hyperventilation in response to long-term hypoxia – Type 1 respiratory failure
– Low pCO2 with initial rise in pH
how many ammonium ions is made fromt he breakdown of glutamine?
2!
which strucutre formed process of breakdown of Glutamine, can freely move across cells? how can it do that?
ammonia!
cuz its uncharged!
how does stomach play a role in making HCO3-?
via alkaline tide!
HCO3- exchanged with CL
so it can make HCL from the H and CL
